The Immune System 4th Edition By Parham Test Bank

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The Immune System 4th Edition By Parham Test Bank



The Immune System 4th Edition By Parham Test Bank



2015 Garland Science


21      Soluble effector molecules are effective when encountering pathogens in/on _____. (Select all that apply.)

  1. extracellular spaces
  2. cytoplasm
  3. epithelial surfaces
  4. interstitial spaces
  5. vesicular compartments
  6. lymph.


22      Which of the three complement pathways becomes activated soonest after an initial infection?

  1. the classical pathway
  2. the lectin pathway
  3. the alternative pathway.


23      Identify the incorrectly paired molecular association.

  1. iC3: factor B
  2. CR4: iC3b
  3. properdin: C3bBb
  4. membrane cofactor protein: C3b2Bb
  5. decay-accelerating factor: C3bBb.


24      All of the following complement proteins help form a pore in the pathogens membrane except _____.

  1. C3b
  2. C5b
  3. C6
  4. C7
  5. C8
  6. C9.


25      The importance of CD59 (also known as protectin) is to _____.

  1. promote the speed of complement activation by protecting C3 convertase C3bBb from proteolytic degradation
  2. prevent the recruitment of C9
  3. dissociate the components of the alternative C3 convertase
  4. prevent the attachment of C3b to host cell surfaces
  5. inhibit the anchoring of C5b, C6, and C7 to host cell surfaces.


26      _____ are soluble complement fragments that mediate localized and systemic inflammatory responses.

  1. cryptdins
  2. defensins
  3. anaphylatoxins
  4. selectins
  5. C-reactive proteins.


27      All of the following statements are correct regarding lpha2-macroglobulin except _____.

  1. it binds covalently to its target via a thioester bond
  2. it possesses a bait region to lure its target
  3. it undergoes a conformational change that enables it to enshroud the target
  4. when bound to its target it is cleared from the circulation by hepatocytes, fibroblasts, and macrophages bearing receptors specific for the complex
  5. its target is the membrane-attack complex on human cells.


28      Although activation of the three different pathways of complement involves different components, the three pathways converge on a common enzymatic reaction referred to as complement fixation.

  1. Describe this reaction.
  2. Describe the enzyme responsible for this reaction in the alternative pathway.
  3. Identify the three effector mechanisms of complement that are enabled by this common pathway.


29      Which of the following is the soluble form of C3 convertase of the alternative pathway of complement activation?

  1. iC3
  2. iC3b
  3. C3b
  4. iC3Bb
  5. C3bBb.


210    Explain the steps that take place when a bacterium is opsonized via C3b:CR1 interaction between the bacterium and a resident macrophage in tissues.


211    In the early stages of the alternative pathway of complement activation there are complement control proteins that are soluble (factors H and I) and associated with the cell surface (DAF and MCP). Identify the (i) soluble and (ii) cell surface-associated complement control proteins that operate in the terminal stages of the alternative pathway of complement activation, and describe their activities.



  1. Review the differences between the three pathways of complement (alternative, lectin, and classical) in terms of how they are activated.
  2. Distinguish which pathway(s) are considered part of an adaptive immune response and which are considered part of innate immunity, and say why.


213    Which of the following does not accurately describe complement components?

  1. soluble proteins
  2. made by the spleen
  3. located in extracellular spaces
  4. some function as proteases once activated
  5. activated by a cascade of enzymatic reactions.


214    Explain why a genetic deficiency of C3 leads to a type of immunodeficiency characterized by recurrent and severe infections.


215    Which of the following is the membrane-bound form of C3 convertase of the alternative pathway of complement activation?

  1. iC3
  2. C3a
  3. C3b
  4. iC3Bb
  5. C3bBb.


216    Explain how the alternative C3 convertase on pathogen cell surfaces is (A) formed and (B) stabilized.


217    Why is it important to expose the hydrophobic sites of C7 and C8 during the formation of the membrane-attack complex?


218    The plasma proteins that counteract the activity of factor P by inactivating C3 convertase through the cleavage of C3b are _____.

  1. factor B and factor H
  2. factor H and factor I
  3. factor B and factor I
  4. decay-accelerating factor and factor H
  5. decay-accelerating factor and membrane cofactor protein.


219    The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are _____.

  1. factor B and factor H
  2. factor H and factor I
  3. factor B and factor I
  4. decay-accelerating factor and factor H
  5. decay-accelerating factor and membrane cofactor protein.


220    Explain the similarities between membrane cofactor protein, factor H, and complement receptor 1 in terms of their complement control properties.


221    Explain how the anaphylatoxins C3a and C5a contribute physiologically to inflammation during complement activation.


222    Which of the following complement components is an opsonin that binds to complement receptor 1 (CR1) on macrophages?

  1. C3b
  2. C3a
  3. Bb
  4. Ba
  5. C3bBb.


223    Which of the following polymerizes to form a transmembrane channel that compromises the integrity of cell membranes?

  1. C5
  2. C6
  3. C7
  4. C8
  5. C9.


224    Which of the following are important in anchoring the membrane-attack complex to the membrane?

  1. C3 and C5
  2. C5 and C6
  3. C6 and C7
  4. C7 and C8
  5. C8 and C9.


225    Which of the following does not contain a glycosylphosphatidylinositol (GPI) lipid tail?

  1. decay-accelerating factor (DAF)
  2. homologous restriction factor (HRF)
  3. membrane cofactor protein (MCP)
  4. protectin (CD59)
  5. all of the above contain a GPI tail.


226    The ligand for CR3 and CR4 formed by the cleavage of C3b by the combined action of factors H and I is called _____.

  1. C3bBb
  2. C3a
  3. C3b2Bb
  4. iC3b
  5. C5b.


227    Which of the following does not describe the actions of the coagulation system?

  1. blood clot formation
  2. enhancement of dissemination of microbes into lymphatics and bloodstream
  3. decrease in blood loss and fluid into interstitial spaces in tissues
  4. release of inflammatory mediators by platelets
  5. wound healing.


228    Damage to tissues triggers a cascade of plasma proteins involving bradykinin and is known as _____.

  1. the alternative pathway of complement
  2. the coagulation system
  3. the kinin system
  4. receptor-mediated endocytosis
  5. the acute-phase response.


229    Which of the following does not describe defensins?

  1. highly conserved with few variants
  2. contain a large proportion of arginine residues
  3. contain three intra-chain disulfide bonds
  4. amphipathic, with hydrophobic and hydrophilic regions
  5. disrupt pathogen membranes by penetrating them and disrupting their integrity.





21      a, c, d, f


22      c


23      d


24      a


25      b


26      c


27      e



  1. The cleavage of C3 into C3a and C3b and the covalent bonding of C3b to the pathogen surface is called complement fixation, and is the reaction on which the alternative, lectin, and classical pathways of complement activation converge.
  2. The enzyme responsible for cleaving C3 into C3a and C3b is called C3 convertase, and it differs in composition depending on the particular complement pathway. The classical and lectin pathways use the classical C3 convertase (C4b2a), whereas the alternative pathway uses the alternative convertase (C3bBb).
  3. C3 is the most abundant complement component in the plasma and circulates as a zymogen, an inactive enzyme. When cleaved into C3a and C3b, three different effector mechanisms are armed: (1) C3b binds to and tags pathogens for destruction by phagocytes through binding to a C3b receptor, CR1; (2) C3b contributes to a multicomponent enzyme, C5 convertase, that catalyzes the assembly of the terminal complement components and the formation of the membrane-attack complex; and (3) C3a is an inflammatory mediator that serves as a chemoattractant and recruits inflammatory cells to the infection site.


29      d


210    The CR1 on the macrophage can bind to C3b that is coating a bacterial surface after complement activation, and the macrophage then engulfs the bacterium through receptor-mediated endocytosis. The macrophage membrane invaginates and forms an intracellular vesicle called a phagosome. The phagosome fuses with a lysosome to form a phagolysosome, where toxic mediators and degradative enzymes are localized. The bacterium is destroyed.



  1. The soluble proteins include S protein, clusterin, and factor J, which all inhibit C5b, C6, and C7 from binding to cell membranes.
  2. The cell surface-associated proteins include homologous restriction factor (HRF) and CD59 (protectin), which both prevent the recruitment of C9 and thus block C9 polymerization.



  1. (1) The classical pathway is activated in two ways, either by the presence of antibody bound to the surface of the microorganism (for example IgM bound to lipopolysaccharide of Gram-negative bacteria) or by the presence of C-reactive protein bound to a bacterium. (2) The lectin pathway requires the presence of mannose-binding lectin, an acute-phase protein made by the liver in response to interleukin-6 (secreted by activated macrophages) and which accumulates in plasma during infection. (3) The alternative pathway requires an activating surface of a pathogen, which stabilizes complement components.
  2. Only the classical pathway is considered part of the adaptive immune response because of the requirement for antibody. However, the classical pathway is also considered part of innate immunity because of the ability of C-reactive protein, an acute-phase protein, to activate it. The other two pathways are considered part of innate immunity because they are initiated independently of antibody.


213    b


214    C3 is a key element in the initiation of the complement cascade in all three pathways of complement activation, namely the alternative, lectin, and classical pathways. Its cleavage into C3a and C3b occurs early in the complement cascade. C3a acts as an inflammatory mediator and recruits inflammatory cells to the site of infection. C3b becomes fixed to the pathogen surface and facilitates the opsonization of pathogens by phagocytes and the assembly of complement components for perforation of the pathogen membrane. In the absence of C3, all three pathways of complement activation would be arrested and extracellular pathogens would escape immune detection until adaptive immune mechanisms develop fully many days later.


215    e



  1. Spontaneous hydrolysis of C3 without cleavage exposes its highly reactive thioester bond, forming iC3. Factor B binds to iC3, is cleaved by factor D, and consequently releases a small fragment called Ba. The larger fragment, Bb, remains associated with iC3 to form iC3Bb, a soluble C3 convertase, which cleaves C3 into C3a and C3b. The reactive thioester bond of C3b is attacked by ROH and RNH2 groups on the surface of the pathogen, where it becomes anchored and binds to factor B. Factor D then cleaves factor B, releasing fragment Ba and forming C3bBb on the pathogen surface.
  2. Factor P (properdin) binds to C3 convertase (C3bBb) bound to the pathogen surface, and inhibits the proteolytic degradation of C3bBb. This stabilizes the C3 convertase and enhances the rate of C3b deposition on the pathogen surface.


217    The hydrophobic sites of C7 and C8 enable anchoring of these two complement components into the membrane of the pathogen. Once anchored in the membrane, the hydrophobic site of C8 facilitates C9 polymerization, which completes the formation of the membrane-attack complex.


218    b


219    e


220    MCP, factor H, and CR1 all bind to C3b and render it susceptible to proteolytic cleavage by factor I. All three contain complement control protein (CCP) modules and are therefore considered regulators of complement activation (RCA).


221    G-protein-coupled receptors for the anaphylatoxins C3a and C5a are found on phagocytes, mast cells, and the endothelial cells of blood vessel walls. Anaphylatoxin bound to mast cells causes them to degranulate, releasing inflammatory mediators such as histamine and leading to increased vascular permeability. Through their action on endothelial cells, anaphylatoxins exert vasoactive effects on blood vessels, contributing to increased vascular permeability and increased blood flow, which facilitate the extravasation of plasma proteins, such as complement proteins and antibodies, and the recruitment of cells to infected tissues through increased adherence and chemotaxis. Phagocytic activity is enhanced by anaphylatoxins, which bring about increased levels of CR1 and CR3 and microbicidal activity. All these activities enhance inflammation.


222    a


223    e


224    d


225    c


226    d


227    b


228    c


229    a




Garland Science 2015

161    Autoimmune diseases, which are classified on the basis of the effector mechanism that causes the symptoms, include all of the following types of hypersensitivity reaction except _____.

  1. type I
  2. type II
  3. type III
  4. type IV.


162    Which type of autoimmune disease is correctly matched with its cause?

  1. type I: IgE-mediated
  2. type II: effector T cells
  3. type III: immune complex deposition in tissues
  4. type IV: extracellular matrix-associated autoantigens
  5. type V: cell-surface components.


163    Match the type of hypersensitivity in column A with its description in column B.

Column A Column B
___ a. type I 1. antibodies directed against extracellular matrix on the cell surface
___ b. type II 2. T cell-mediated
___ c. type III


3. deposition of soluble immune complexes in tissues
___ d. type IV 4. IgE-mediated



164    Which of the following is an example of a type II autoimmune response? (Select all that apply.)

  1. subacute bacterial endocarditis
  2. Goodpastures syndrome
  3. multiple sclerosis
  4. systemic lupus erythematosus
  5. myasthenia gravis.


165    Which of the following is an example of a type III autoimmune response? (Select all that apply.)

  1. mixed essential cryoglobulinemia
  2. acute thrombocytopenia purpura
  3. systemic lupus erythematosus
  4. rheumatoid arthritis
  5. insulin-resistant diabetes.


166    Which of the following is an example of a type IV autoimmune response? (Select all that apply.)

  1. pemphigus vulgaris
  2. autoimmune thrombocytopenia purpura
  3. subacute bacterial endocarditis
  4. type 1 diabetes
  5. multiple sclerosis.


167    Explain why splenectomy is sometimes carried out in patients with persistent type II autoimmune diseases that affect leukocytes.


168    If autoantibodies of the IgG or IgM isotype were produced with specificity for components found on the surface of erythrocytes, which of the following would occur? (Select all that apply.)

  1. formation of membrane-attack complex
  2. immune-complex deposition in renal glomeruli
  3. anemia
  4. hypothyroidism
  5. receptor-mediated phagoytosis via Fc receptors on phagocytes.


169    Which of the following is the cause of red blood cell deficiency in autoimmune hemolytic anemia? (Select all that apply.)

  1. inability of red blood cells to develop normally in the bone marrow
  2. loss of red blood cells due to widespread pinpoint hemorrhages
  3. hemolysis by assembly of membrane-attack complexes
  4. phagocyte-mediated clearance in the spleen
  5. rapid turnover of red blood cells due to CD8 T-cell killing.


1610  All of the following are associated with Goodpastures syndrome except _____. (Select all that apply.)

  1. chain of type IV collagen
  2. inflammation
  3. extracellular matrix antigen
  4. neutropenia
  5. renal tubules and glomeruli
  6. type III hypersensitivity reaction.


1611  _____ is a highly variable type III autoimmune disease in which immune complexes form and may cause glomerulonephritis of the kidney, arthritis of the joints, and vasculitis of the face.

  1. pemphigus vulgaris
  2. systemic lupus erythematosus
  3. rheumatoid arthritis
  4. multiple sclerosis
  5. Goodpastures syndrome.


1612  Individuals who have two defective alleles of the AIRE gene _____.

  1. exhibit symptoms of autoimmunity at a young age
  2. are unable to activate regulatory T cells
  3. exhibit decreased predisposition to autoimmune disease
  4. are very effective at inducing anergy of circulating autoreactive B and T cells
  5. are more likely to be women of African or Asian origin.


1613  All of the following autoimmune diseases are correctly matched with their HLA disease associations except _____.

  1. HLA-B27: ankylosing spondylitis
  2. HLA-DQ2: type 1 diabetes in Africans and Asians
  3. HLA-B35: birdshot retinopathy
  4. HLA-DR4: rheumatoid arthritis
  5. HLA-DQ6: narcolepsy.


1614  The haplotype A1B8DR3DQ2 is associated with several common autoimmune diseases including all of the following except _____.

  1. ankylosing spondylitis
  2. systemic lupus erythematosus
  3. autoimmune hepatitis
  4. myasthenia gravis
  5. type 1 diabetes
  6. primary biliary cirrhosis.


1615  With the exception of ______, these autoimmune diseases are more prevalent in women than in men.

  1. rheumatoid arthritis
  2. multiple sclerosis
  3. ankylosing spondylitis
  4. Sjgrens syndrome
  5. Graves disease.


1616  Which of the following is not a characteristic of Graves disease?

  1. weight loss
  2. enlarged thyroid gland
  3. elevated thyroid-stimulating hormone
  4. heat intolerance
  5. overproduction of T3 and T4.


1617  All of the following are true regarding thyroglobulin except _____.

  1. its tyrosine residues are iodinated and cross-linked
  2. it is broken down to produce thyroid hormones
  3. it is stored in follicles of the thyroid
  4. it signals the pituitary gland to stop releasing thyroid-stimulating hormone
  5. it is synthesized initially as a glycoprotein by thyroid epithelial cells.


1618  Which of the following describes myasthenia gravis?

  1. Ectopic lymphoid tissue forms and impairs endocrine function.
  2. Disruption of adhesion molecules of cellular junctions.
  3. Autoimmune response to proteins of anterior chamber of the eye.
  4. Chronic inflammation of the gut mucosa.
  5. The neuromuscular junction is compromised.


1619  Which of the following is associated with antagonistic autoantibodies against cell-surface receptors or adhesion molecules? (Select all that apply.)

  1. myasthenia gravis
  2. rheumatoid arthritis
  3. insulin-resistant diabetes
  4. Graves disease
  5. pemphigus vulgaris.


1620  The reason why babies born to mothers with Graves disease suffer passively from the disease for only a short while after birth is that _____.

  1. very little IgM is transported across the placenta
  2. only antibodies, and not the B cells making the autoantibodies, cross the placenta
  3. the newborns regulatory T cells suppress autoantibody production
  4. the newborns thyroid gland develops resistance to the effects of maternal autoantibodies
  5. thyroglobulin synthesis does not commence until months after birth.


1621  The formation of ectopic lymphoid tissues occurs in all of the following conditions except _____.

  1. pemphigus foliaceus
  2. chronic hepatitis C infection
  3. Hashimotos disease
  4. rheumatoid arthritis
  5. multiple sclerosis
  6. Graves disease.


1622  A(n) _____ binds to the antigen-binding site of another antibody.

  1. cryptic epitope
  2. anti-idiotypic antibody
  3. molecular mimic
  4. receptor antagonist
  5. autoantibody.


1623  All of the following are linked to the development of rheumatoid arthritis or are associated with its treatment except _____. (Select all that apply.)

  1. anti-immunoglobulin autoantibodies
  2. adalumumab
  3. leukocyte infiltration in synovial tissue
  4. joint inflammation
  5. pulmonary hemorrhage
  6. rituximab
  7. increased susceptibility if the person possesses the HLA-DRB1*04:01 or 04:04 allotypes.
  8. peptidyl arginine deiminases
  9. smoking
  10. rheumatic fever.


1624  It is believed that the allotype DRB1*_____ may confer protection against rheumatoid arthritis because it contains _____ amino acid residues at positions 70 and 71 that bind to different subsets of peptides compared with the allotypes that confer susceptibility to this disease.

  1. 04:01; acidic
  2. 04:02; acidic
  3. 04:04; basic
  4. 04:05; basic

e          04:08; acidic.


1625  Celiac disease exhibits all of the following symptoms except _____.

  1. villous atrophy
  2. anemia
  3. diarrhea
  4. tissue ulceration
  5. malabsorption
  6. increased susceptibility to intestinal cancer.


1626  All of the following are characteristics of tissue transglutaminase except ____.

  1. generation of negatively charged peptides that bind well to the positively charged pockets of the DQ2 and DQ8 allotypes
  2. conversion of glutamine to glutamate by deamination
  3. upregulation during tissue inflammation
  4. stimulation of IgG or IgA autoantibodies in celiac disease
  5. predisposition to celiac disease if individual possesses particular polymorphic variants.


1627  Describe three types of unwanted and potentially harmful immune response.


1628  Which of the following describes processes by which self-reactive lymphocytes are rendered incapable of mounting an autoimmune response? (Select all that apply.)

  1. sequestration of autoantigens in immunologically privileged sites
  2. induction of anergy in peripheral compartments
  3. positive selection of autoimmune T lymphocytes in secondary lymphoid tissues
  4. negative selection of T lymphocytes in the thymus
  5. suppression by regulatory T cells
  6. negative selection of B lymphocytes in the bone marrow
  7. expression of AIRE in the bone marrow
  8. induction of alloreactive responses it the thymus
  9. somatic hypermutation to an alternative antigen specificity
  10. apoptosis in primary lymphoid tissue
  11. deprivation of T-cell help.


1629  From Table 1629 below, match the autoimmune disease in column A with the corresponding antigen in column B and the consequence in column C. Use each answer only once. Then indicate whether the autoimmune disease is categorized as type II, III, or IV.

Table Q1629
Column A Column B Column C
a. Rheumatoid arthritis 1. Myelin basic protein, proteolipid protein A. Destruction of red blood cells by complement and phagocytosis, anemia
b. Subacute bacterial endocarditis 2. DNA, histones, ribosomes, snRNP, scRNP B. Joint inflammation and destruction
c. Autoimmune hemolytic anemia 3. Thyroid-stimulating hormone receptor C. Pancreatic cell destruction
d. Mixed essential cryoglobulinemia 4. Bacterial antigen D. Glomerulonephritis
e. Multiple sclerosis 5. Rheumatoid factor IgG complexes E. Hyperthyroidism
f. Systemic lupus erythematosus 6. Epidermal cadherin F. Blistering of skin
g. Type 1 diabetes 7. Synovial joint antigen G. Glomerulonephritis, vasculitis, arthritis
h. Graves disease 8. Rh blood group antigens H. Systemic vasculitis
i. Pemphigus vulgaris 9. Pancreatic cell antigen I. Brain degeneration, paralysis


1630  Describe the three immunological mechanisms responsible for the destruction of red blood cells in autoimmune hemolytic anemia.


1631  Characterize two properties of endocrine glands that render them susceptible to autoimmune attack.


1632  Hashimotos and Graves diseases both impair normal functioning of the thyroid gland but do so using different immunopathological mechanisms. Compare and contrast these mechanisms.


1633  Indicate whether each of the following statements is true (T) or false (F).

___a. During pregnancy, IgG antibodies and activated lymphocytes can cross the placenta and enter the circulatory system of the fetus.

___b. Blood plasma exchange (plasmapheresis) can be used to remove maternal IgG from the newborn.

___c. All autoimmune diseases involve a breach of T-cell tolerance.

___d. Newborns of mothers with T cell-mediated autoimmune diseases exhibit the same symptoms as their mothers.

___e. Autoimmune diseases can be induced after an infection.



  1. What mechanism of self-tolerance is broken in the autoimmune syndrome APECED?
  2. What is the underlying genetic defect in APECED? Explain why it leads to a reduction in self-tolerance.


1635  You have isolated a subset of CD25+ CD4+ T cells from the blood that have T-cell receptors specific for a self antigen but do not proliferate when challenged with the antigen in vitro. What is the name given to these T cells, and what role are they thought to have in preventing autoimmunity?


1636  People who are heterozygous for HLA-DQ2 and HLA-DQ8 allotypes are at greater risk of developing type 1 diabetes than those who are homozygous for HLA-DQ2 or HLA-DQ8.

  1. Explain the reason for this increased susceptibility.
  2. Why is the above statement true mainly for people of northern European origin but not for some other ethnic groups?



  1. Which patients affected by Goodpastures syndrome also succumb to pulmonary hemorrhage?
  2. Explain the reason for this complication.


1638  Explain the relationship between HLA-DRB1*04, smoking, the expression of peptidyl arginine deaminase, and rheumatoid arthritis.


1639  In the context of autoimmunity: (A) define molecular mimicry; and (B) provide an example.


1640  A recent therapy developed for the treatment of rheumatoid arthritis includes the use of _____ monoclonal antibodies that suppress the autoimmune response. (Select all that apply.)

  1. anti-TNF-
  2. anti-C-reactive protein
  3. anti-CD20
  4. anti-rheumatoid factor
  5. anti-CD3.


1641  Chronic diseases in which the immune response is targeted toward autologous entities of ones body are known as _____.

  1. hypersensitivity reactions
  2. innate immune reactions
  3. allergic reactions
  4. autoimmune diseases
  5. anergic reactions.


1642  Discuss why splenectomy is a viable treatment for chronic autoimmune diseases targeted at circulating neutrophils.


1643  Indicate whether each of the following statements is true (T) or false (F).

___ a. Autoimmune diseases are rarely resolved.

___ b. Autoimmune responses are the result of innate immune responses directed toward self antigens.

___ c. Some forms of autoimmune disease involve IgE autoantibodies.

___ d. During pregnancy the fetus is exposed to maternal leukocytes.

___ e. Ectopic lymphoid tissue resembling secondary lymphoid tissue may develop under the influence of lymphotoxin (LT).


1644  Match the autoimmune disease in column A with the consequence in column B.

Column A Column B
___ a. type 2 diabetes 1. skin blistering
___ b. rheumatoid arthritis 2. joint deterioration
___ c. mixed essential cryoglobulinemia 3. keotacidosis
___ d. acute rheumatic fever 4. heart valve scarring
___ e. pemphigus vulgaris 5. systemic vasculitis



Match the autoimmune disease in column A with the autoantigen in column B.

Column A Column B
___ a. mixed essential cryoglobulinemia 1. thyroid-stimulating hormone receptor
___ b. myasthenia gravis 2. cell wall components of Streptococcus
___ c. Graves disease 3. myelin basic protein
___ d. acute rheumatic fever 4. acetylcholine receptor
___ e. multiple sclerosis 5. rheumatoid factor IgG


1646  Which of the following would be consistent with a diagnosis of Goodpastures syndrome? (Select all that apply.)

  1. pulmonary hemorrhage
  2. joint inflammation
  3. glomerulonephritis
  4. anti-collagen IgG deposition in renal glomeruli
  5. hyperglycemia.


1647  Thyroid-stimulating hormone is made in the _____ and induces the release of thyroid hormones after proteolytic processing of _____.

  1. pituitary gland; thyroglobulin
  2. hypothalamus; thyroxine
  3. pancreas; thyroglobulin
  4. pituitary gland; thyroid-stimulating hormone receptor
  5. thyroid gland; thyroid peroxidase.


1648  Graves disease causes _____, whereas Hashimotos disease causes _____.

  1. hypothyroidism; hyperthyroidism
  2. hyperthyroidism; hypothyroidism
  3. hypoglycemia; hyperglycemia
  4. hyperglycemia; hypoglycemia
  5. glomerulonephtitis; systemic vasculitis.



  1. What is ectopic lymphoid tissue?
  2. Give four examples where this type of tissue forms in autoimmune disease.


1650  How do the treatments for Hashimotos and Graves diseases differ, and why?


1651  Which of the following are correctly matched? (Select all that apply.)

  1. exocrine tissue: islets of Langerhans
  2. type 2 diabetes: insulin-dependent diabetes mellitus
  3. cells of pancreas: insulin production
  4. cells of pancreas: somatostatin production
  5. insulitis: lymphocyte infiltration in islets of Langerhans.


1652  Examples of rheumatic diseases caused by autoimmune responses include _____. (Select all that apply.)

  1. rheumatoid arthritis
  2. acute rheumatic fever
  3. multiple sclerosis
  4. autoimmune hemolytic anemia
  5. Sjgrens syndrome
  6. systemic lupus erythematosus.


1653  Another name for anti-immunoglobulin autoantibodies is _____.

  1. C-reactive protein
  2. rheumatoid factor
  3. rituximab
  4. thyroglobulin
  5. ectopic antibodies
  6. infliximab.


1654  Rituximab, used in the treatment of rheumatoid arthritis, depletes _____ through a process involving the cross-linking of _____ on the surface of NK cells and the induction of antibody-dependent cell-mediated cytotoxicity.

  1. NK cells; NKG2D
  2. T cells: NKG2D
  3. inflammatory cytokines; TNF-alpha
  4. C-reactive protein; FcRIII
  5. B cells; FcRIII.


1655  Which of the following autoimmune diseases affect the nervous system? (Select all that apply.)

  1. myasthenia gravis
  2. mixed essential cryoglobulinemia
  3. Graves disease
  4. pemphigus vulgaris
  5. multiple sclerosis.


1656  _____ autoantibodies enhance receptor function.

  1. neutralizing
  2. opsonizing
  3. agonist
  4. complement-fixing
  5. antagonist.


1657  Antagonistic autoantibodies made against the insulin receptor cause _____. (Select all that apply.)

  1. type 1 diabetes
  2. hypoglycemia
  3. hyperglycemia
  4. insulin-resistant diabetes
  5. light-headedness.


1658  Deficiency in the production of AIRE results in _____. (Select all that apply.)

  1. normal expression of tissue-specific proteins in the bone marrow and thymus
  2. incomplete negative selection of developing T cells
  3. the development of autoimmune B-cell and T-cell responses against endocrine glands and other tissues
  4. death in infancy
  5. the development of autoimmune polyendocrinopathycandidiasisectodermal dystrophy (APECED).


1659  Describe two different ways in which infection with bacteria or viruses compromises T-cell tolerance, leading to the production of effector T cells specific for self antigens.


1660  Ankylosing spondylitis has a strong association with polymorphisms found in _____.

  1. HLA-B27
  2. AIRE
  3. CTLA-4
  4. HLA-DQ6
  5. HLA-Cw6
  6. FoxP3
  7. TNF-.


1661  Autoantibody specificities are affected by HLA class II polymorphisms. In the case of systemic lupus erythematosus, indicate which of the following associations between HLA-class II and autoantigens have been observed in these patients.

  1. HLA-DR3; nuclear ribonucleoprotein complex
  2. HLA-DR5; small cytoplasmic ribonucleoprotein complex
  3. HLA-DR2; double-stranded DNA
  4. HLA-DR4; single-stranded RNA
  5. HLA-DQ8; double-stranded RNA.


1662  Explain the mechanism that gives rise to a broadening B-cell response during the course of systemic lupus erythematosus.


1663  _____ is an example in which physical trauma provides access of lymphocytes to an otherwise immunologically privileged site. (Select all that apply.)

  1. rheumatoid arthritis
  2. multiple sclerosis
  3. type 1 diabetes
  4. myasthenia gravis
  5. sympathetic ophthalmia.


1664  Bacterial infections are associated with which of the following autoimmune diseases? (Select all that apply.)

  1. Reiters syndrome
  2. pemphigus vulgaris
  3. reactive arthritis
  4. rheumatic fever
  5. myasthenia gravis.


1665  _____ is the term used to describe how pathogen antigens resemble host antigens and can sometimes trigger autoimmune disease.

  1. intramolecular epitope spreading
  2. molecular mimicry
  3. intermolecular epitope spreading
  4. sympathetic senescence
  5. linkage equilibrium.



  1. What is meant by the term epitope spreading?
  2. Name one autoimmune disease affecting the skin in which epitope spreading is involved, and explain how.


1667  The upregulation of _____ by IFN- can contribute to antigen-specific T-cell activation on thyroid epithelium.

  1. CD4
  2. CD8
  3. HLA class I
  4. HLA class II
  5. CD28.


1668  A(n) _____ is an epitope that is typically not accessible to the immune system but is revealed under inflammatory or infectious states.

  1. cryptic epitope
  2. molecular mimic
  3. regulatory peptide
  4. carrier
  5. adjuvant.


1669  The process by which the human thymus gradually decays is known as _____.

  1. apoptosis
  2. senescence
  3. involution
  4. the hygiene hypothesis
  5. self-tolerance.


1670  The autoreactive CD4 T cells of elderly people with rheumatoid arthritis _____. (Select all that apply.)

  1. express high levels of CD28
  2. are predominantly anergic
  3. express KIR2DS2
  4. are highly susceptible to apoptosis in inflamed joints
  5. produce IFN-.


1671  Amanda Chenoweth, 21 years of age, returned from a summer job as a pianist on a cruise ship where she was exposed daily to excessive sun; she developed a rash on her cheeks. She complained that her finger joints were stiff and painful, which made it difficult to play the piano, and that her hips became painful after sitting at the piano for long periods. Her blood sample tested positive for anti-nuclear antibodies and had decreased serum C3 levels. A urine albumin test showed elevated protein levels. A course of prednisone (an anti-inflammatory steroid) in combination with naprosyn (a nonsteroidal anti-inflammatory agent) was begun and her condition improved rapidly. What is the most likely cause and clinical name of her condition?

  1. deterioration of the central nervous system; multiple sclerosis
  2. cartilage destruction by bone-cell enzymes; rheumatoid arthritis
  3. immune complexes fixing complement in kidney, joints, and blood vessels; systemic lupus erythematosus
  4. autoantibodies against acetylcholine receptor at the neuromuscular junction; myasthenia gravis
  5. consumption of seafood to which she was allergic; acute systemic anaphylaxis.


1672  At 42 years old, Stephanie Goldstein developed occasional blurred and double vision, numbness and pins and needles in her arms and legs (paresthesia), and bladder incontinence. After a month of these symptoms she went to her doctor, who sent her to the neurology specialist. An MRI scan revealed areas of demyelination in the central nervous system (CNS), and Stephanie was diagnosed with the autoimmune disease multiple sclerosis (MS). Which of the following best explains why some people are susceptible to the development of MS?

  1. Negative selection of autoreactive T cells occurs during T-cell development.
  2. Apoptosis of autoreactive B cells occurs in the bone marrow during B-cell development.
  3. An inability to produce immunological tolerance toward CNS-derived constituents results in the generation of self-reactive lymphocytes.
  4. An immunodeficiency inhibiting somatic recombination of immunoglobulins and T-cell receptors results in impaired lymphocyte development.
  5. Regulatory T cells fail to activate autoreactive T cells in secondary lymphoid organs.


1673  Anders Anderson, was seen by his pediatrician at 24 months old after a recent bout of diarrhea and vomiting. He had lost his appetite and complained that his stomach hurt. Anders was in the 5% centile for weight, had slender limbs, wasted buttocks, and a protuberant abdomen. Jejunal biopsy revealed abnormal surface epithelium, and villous atrophy with hyperplasia of the crypts. Which of the following would be a likely clinical finding in this patient?

  1. glomerulonephritis
  2. urticarial rash
  3. anti-gliadin IgA antibodies
  4. chronic wheezing
  5. low blood pressure.


1674  Seventeen-year-old Lisa Montague practiced piano for 34 hours each day while preparing for music college auditions. Some of her pieces required sustained arm-muscle activity and she began to find them hard to play, even though she had previously played them easily. When she also started to have difficulty swallowing and chewing, she told her mother, who took her to the emergency room, where the physician noticed drooping eyelids and limitation of ocular motility. An electromyogram detected impaired nerve-to-muscle transmission. Administration of pyridostigmine rapidly improved Lisas symptoms. Which of the following blood-test results would be most consistent with her condition?

  1. elevated rheumatoid factor
  2. elevated anti-myelin basic protein antibodies
  3. elevated anti-acetylcholine receptor antibodies
  4. elevated anti-nuclear antibodies
  5. elevated anti-Rh antibodies.








161    a


162    c


163    a4; b1; c3; d2


164    b, e


165    a, c


166    d, e


167    When autoantibodies directed toward leukocyte surface antigens bind to the cell surface, complement fixation and deposition of C3b occurs. The membrane-attack complex usually does not form on leukocytes because of complement regulatory proteins. Their elimination from the circulation, however, occurs by a different mechanism involving splenic macrophages that bear FcR and CR1, receptors for antibodies and C3b, respectively. The macrophages carry out phagocyte-mediated clearance of these leukocytes, leading to a deficiency of these cells in the circulation. Removal of the spleen spares the elimination of these leukocytes. The presence of antibody and C3b on their cell surface does not affect their ability to functional normally.


168    a, c, e


169    c, d


1610  d, f


1611  b


1612  a


1613  c


1614  a


1615  c


1616  c


1617  d


1618  e


1619  a, c, e


1620  b

1621  a


1622  b


1623  e, j


1624  b


1625  d


1626  e



(i) Allergy. IgE antibodies made against normally innocuous environmental antigens trigger widespread mast-cell activation. This can lead to allergic diseases such as asthma or to a potentially fatal anaphylactic reaction.

(ii) Autoimmune disease. Chronic immune responses by B cells or T cells to self antigens can cause tissue damage and chronic illnesses such as diabetes, multiple sclerosis, and myasthenia gravis. Autoimmunity is sometimes provoked as a consequence of an immune response to pathogen-derived antigen that cross-reacts on healthy host cells or tissue.

(iii) Transplant rejection. A persons immune system will make an immune response against the foreign MHC molecules on transplanted tissue that is MHC-incompatible.


1628  a, b, d, e, f, j, k



  1. Rheumatoid arthritis: 7, B IV
  2. Subacute bacterial endocarditis: 4, D III
  3. Autoimmune hemolytic anemia: 8, A II
  4. Mixed essential cryoglobulinemia: 5, H III
  5. Multiple sclerosis: 1, I IV
  6. Systemic lupus erythematosus: 2, G III
  7. Type 1 diabetes: 9, C IV
  8. Graves disease: 3, E II
  9. Pemphigus foliaceus: 6, F II


1630  (i) Red blood cells coated with antibodies against red blood cell-surface components bind to splenic macrophages via Fc receptors, inducing phagocytosis of the red blood cell by receptor-mediated endocytosis. (ii) Red blood cells bound by antibodies against red blood cells fix complement, which causes deposition of C3b on the surface of the red blood cell. C3b then binds to the receptor CR1 on splenic macrophages, inducing phagocytosis of red blood cells. (iii) Antibody against red blood cells triggers the complement cascade and the formation of membrane-attack complexes on the red blood cell, leading to cell lysis.


1631  First, endocrine glands synthesize tissue-specific proteins unique to that gland. These proteins are not normally found in primary lymphoid organs where lymphocyte maturation occurs. Hence, the population of T and B lymphocytes is not tolerant to some endocrine gland-specific proteins, and these self proteins are thus recognized as foreign antigens. Second, endocrine glands are highly vascularized because their products need to gain access to the circulation. This feature gives leukocytes relatively easy access to endocrine tissue.


1632  Both Hashimotos and Graves diseases disrupt the normal production of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4), which are derived from thyroglobulin in thyroid follicles. The formation of T3 and T4 requires engagement of the thyroid-stimulating hormone receptor (TSHR) with thyroid-stimulating hormone (TSH) secreted from the pituitary gland, a key step in the regulation of thyroid hormone production. This step malfunctions for these two diseases.

In Hashimotos disease, anti-thyroid antigen antibodies and TH1 effector cells are involved. Large numbers of lymphocytes take up residence in the gland tissue, establishing germinal centers that resemble those in lymph nodes. Eventually the thyroid tissue is destroyed and thyroid follicles are no longer able to respond to TSH and make T3 or T4, a condition called hypothyroidism.

Graves disease, in contrast, results in hyperthyroidism. Anti-TSHR antibodies act agonistically, mimicking TSH even in its absence. The thyroid follicle is chronically overstimulated by these antibodies and overproduces T3 and T4. The effector T cells are of the TH2 type, and the absence of lymphocyte infiltration retains the thyroid gland in operable condition. Therefore T3 and T4, no longer regulated by TSH, are secreted continuously in excess of concentrations required by the body.


1633  aF; bT; cT; dF; eT



  1. The negative selection of developing autoreactive T cells in the thymus.
  2. The underlying genetic defect is in a gene encoding a protein called AIRE (autoimmune regulator). This is a transcription factor that, when working normally, causes several hundreds of proteins otherwise expressed only in particular peripheral tissues to be expressed by medullary epithelial cells in the thymus. This induces the negative selection of T cells specific for these proteins and their deletion from the T-cell repertoire. The T cells emerging from the thymus are therefore tolerant to a large number of antigens found primarily on organs and tissues elsewhere in the body. When AIRE is defective and these proteins are not expressed in the thymus, the population of naive T cells that develops will contain T cells reactive against these antigens of peripheral tissues.


1635  These cells are called regulatory T cells (Treg). When activated by encounter with their corresponding self antigen, they become able to suppress the activation of naive autoreactive T cells. This active suppression of autoreactive T cells in the periphery is now thought to be an important method of preventing autoimmune reactions.



  1. Increased risk of developing type 1 diabetes is associated with the formation of a heterozygote-specific heterodimer composed of the HLA-DQ8 chain DQA1*03 and the HLA-DQ2 chain DQB1*02:01.
  2. In northern Europeans this combination of and chains is never encoded in the same haplotype, so it can be produced only in heterozygotes. Haplotypes containing both susceptibility alleles can, however, be present in Africans, and similarly confer susceptibility to type 1 diabetes.



  1. Habitual cigarette smokers with Goodpastures syndrome develop not only glomerulonephritis but also pulmonary hemorrhage.
  2. Unlike non-smokers, whose basement membranes are in general not compromised in pulmonary alveoli, smokers have alveoli that are damaged as a result of chronic exposure to cigarette smoke. Damage provides a gateway by which autoantibodies can gain access to basement membranes, where they become deposited, activate complement, and cause rupture of alveolar blood vessels.


1638  Peptidyl arginine deaminase (PAD) is an enzyme induced in the respiratory tract after smoke-induced damage. PAD converts arginine residues in self proteins to citrulline residues, thus creating epitopes to which the T-cell repertoire is not tolerant. Citrullinated proteins are subject to proteolysis, and the resulting peptides bind to HLA-DRB1*04 and stimulate autoreactive CD4 T cells and antibodies against citrullinated self proteins. If a joint becomes infected or is wounded, inflammation of joint tissue activates PAD, which generates the same citrullinated epitopes. HLA-DRB1*04-restricted effector and memory T cells are recruited and activated and an immune response follows, initiating the development of rheumatoid arthritis.



  1. Molecular mimicry refers to the phenomenon in which a pathogen expresses an antigen that bears a chemical similarity to a host-cell antigen. Once pathogen-specific antibodies or effector T cells are generated, they have the potential to cross-react with self antigen.
  2. An autoimmune disease involving molecular mimicry is rheumatic fever. Infection with Streptococcus pyogenes (for example strep throat) results in the production of antibodies specific for the bacterial cell-wall proteins. These antibodies cross-react with chemically similar (but not identical) self antigen expressed on heart tissue. This is followed by complement activation and the production of inflammatory mediators, which cause damage to heart tissue and valves and the formation of scar tissue, which can lead to cardiovascular complications later in life. This type of immunological aftermath can be avoided if antibiotics are administered early during infection.


1640  a, c


1641  d


1642  Neutrophils targeted by autoantibodies are predominantly destroyed in the spleen through uptake by splenic macrophages via Fc receptors and the complement receptor CR1. Splenectomy would thus reduce the rate at which neutrophils are destroyed. By themselves, antibodies and complement bound to the neutrophil surface do not impair the normal function of neutrophils. In addition, white blood cells are far less susceptible to the formation of membrane-attack complement complexes, owing to the continual production of complement regulatory proteins in these nucleated cells.


1643  aT; bF; cF; dF; eT


1644  a3; b2; c5; d4; e1


1645  a5; b4; c1; d2; e3


1646  a, c


1647  a


1648  b



  1. Ectopic lymphoid tissue, also known as tertiary lymphoid tissue, is found as a result of infiltration of immune-system cells, such as lymphocytes, dendritic cells, macrophages, and follicular dendritic cells, into endocrine tissue. The cells then organize through a process known as lymphoid neogenesis to form structures that functionally resemble secondary lymphoid tissues, except that ectopic lymphoid tissue lacks a capsule and does not associate with the lymphatics.
  2. Ectopic lymphoid tissue is characteristic of Hashimotos thyroiditis and has also been associated with rheumatoid arthritis, Graves disease, and multiple sclerosis.


1650  Hashimotos and Graves diseases are treated differently because, although they both affect the thyroid gland, they exert opposing effects on the production of thyroid hormonesinhibition and overproduction, respectively. Hashimotos disease is treated by administering synthetic thyroid hormones orally to replace the deficiencies in T3 and T4. Graves disease is treated either by suppressing thyroid function with inhibitory drugs or by thyroidectomy combined with thyroid hormone replacement therapy.


1651  c, e


1652  a, e, f


1653  b


1654  e


1655  a, e


1656  c


1657  c, d


1658  b, c, e



(i) Inflammatory cytokines induced by infection can activate autoreactive T cells nonspecifically, and interfere with the ability of regulatory T cells to maintain peripheral tolerance.

(ii) T-cell cross-reactivity can occur when pathogen peptides have related amino acid motifs compared with self peptides and, when bound to the same or similar MHC allotype, can lead to the activation of self-reactive T cells. In some cases the only requirement is a common peptide:MHC structural conformation and neither peptide nor MHC relatedness is actually required. In both cases, however, molecular mimicry is operating.


1660  a


1661  c


1662  In SLE, the protein epitopes recognized by autoreactive T cells are part of large macromolecular complexes composed of aggregates of histone proteins and DNA, or aggregates of ribosomal proteins and RNA. Accessible epitopes on the external surface of the complex can bind easily to antigen receptors on the surface of different neighboring B cells that possess different epitope specificities (for example histone-specific antigen receptors as well as DNA-specific antigen receptors). If these B cells are presenting peptides to which the original autoreactive CD4 T cells is specific, then help is provided to both types of B cell and antibodies are generated to both accessible epitopes. Alternatively, if the B cell internalizes and degrades the complex and presents peptides derived from inaccessible interior proteins to CD4 T cells, then T cells with specificities to all protein components of the complex, both accessible and inaccessible, become activated and the immune response broadens.


1663  a, e


1664  a, c, d


1665  b



  1. Epitope spreading is the phenomenon in which the immune response, having initially targeted a particular epitope on an antigen molecule, progressively involves other cross-reactive epitopes on the same molecule.
  2. Pemphigus foliaceus. Autoantibody production against the protein desmoglein, a component of desmosomes, initially involves epitopes that do not result in any tissue damage or symptoms. Only when additional desmoglein epitopes become involved, as a result of epitope spreading, does the autoimmune response cause damage to desmosomes and give rise to lesions in the skin (the disease pemphigus).


1667  d


1668  a


1669  c


1670  c, e


1671  Rationale: The answer is c. This is a case of systemic lupus erythematosus (SLE). The vascular rash on the face, and the painful finger joints and hips, suggest that Amanda has developed a systemic inflammatory condition. The decreased levels of C3 are consistent with increased complement fixation by the classical pathway mediated by the anti-nuclear antibodies typical of SLE. Elevated levels of protein in the urine are suggestive of glomerulonephritis, another common complication of SLE. When immune complexes of antibody, complement, and antigen are deposited in the synovia of joints, in blood vessel walls, and in kidney glomeruli rather than being cleared from the circulation, inflammation results.


1672  Rationale: The correct answer is c. One mechanism for achieving immunological tolerance to self proteins is negative selection in the thymus. Developing T cells bearing T-cell receptors that bind too strongly to self MHC or to self-peptide:self-MHC complexes are signaled to die by apoptosis, which eliminates self-reactive T cells. Self proteins not presented to developing T cells in the thymus, such as proteins sequestered in the central nervous system, would not be scrutinized during negative selection, and self-reactive T cells would result.


1673  Rationale: The correct answer is c. This is a case of celiac disease, also known as gluten-sensitive enteropathy. An inflammatory response involving CD4 T cells is made against gluten proteins (including gliadins and glutenins) in gut-associated lymphoid tissues. Anti-gliadin and anti-glutenin IgA antibodies are secreted into the lumen of the gut. Atrophy of intestinal villi compromises absorption and, as seen in this case, affected children fail to thrive.


1674  Rationale: The correct answer is c. This is a case of myasthenia gravis, a type II autoimmune disease caused by antagonist antibodies against acetylcholine receptors, which impede the binding of the neurotransmitter acetylcholine. Lisa experienced muscle weakness and impairment of neuromuscular signaling, which affected the strength in oral, ocular, and upper extremity muscles, hallmarks of this disease. Pyridostigmine is an inhibitor of cholinesterase, an enzyme that normally degrades acetylcholine after neuromuscular transmission. That Lisa demonstrated rapid recovery when treated with this drug shows that acetylcholine was associated with her symptoms, and by increasing the acetylcholine concentration her symptoms were alleviated.



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