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THE IMMUNE SYSTEM, FOURTH EDITION
CHAPTER 2: INNATE IMMUNITY: THE IMMEDIATE RESPONSE TO INFECTION
2015 Garland Science
21 Soluble effector molecules are effective when encountering pathogens in/on _____. (Select all that apply.)
22 Which of the three complement pathways becomes activated soonest after an initial infection?
23 Identify the incorrectly paired molecular association.
24 All of the following complement proteins help form a pore in the pathogens membrane except _____.
25 The importance of CD59 (also known as protectin) is to _____.
26 _____ are soluble complement fragments that mediate localized and systemic inflammatory responses.
27 All of the following statements are correct regarding lpha2-macroglobulin except _____.
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.
29 Which of the following is the soluble form of C3 convertase of the alternative pathway of complement activation?
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.
213 Which of the following does not accurately describe complement components?
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?
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 _____.
219 The membrane-bound proteins on human cells that dissociate and inactivate alternative C3 convertase to avoid complement activation are _____.
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?
223 Which of the following polymerizes to form a transmembrane channel that compromises the integrity of cell membranes?
224 Which of the following are important in anchoring the membrane-attack complex to the membrane?
225 Which of the following does not contain a glycosylphosphatidylinositol (GPI) lipid 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 _____.
227 Which of the following does not describe the actions of the coagulation system?
228 Damage to tissues triggers a cascade of plasma proteins involving bradykinin and is known as _____.
229 Which of the following does not describe defensins?
21 a, c, d, f
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.
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.
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.
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.
THE IMMUNE SYSTEM, FOURTH EDITION
CHAPTER 16: DISRUPTION OF HEALTHY TISSUE BY THE ADAPTIVE IMMUNE RESPONSE
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 _____.
162 Which type of autoimmune disease is correctly matched with its cause?
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.)
165 Which of the following is an example of a type III autoimmune response? (Select all that apply.)
166 Which of the following is an example of a type IV autoimmune response? (Select all that apply.)
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.)
169 Which of the following is the cause of red blood cell deficiency in autoimmune hemolytic anemia? (Select all that apply.)
1610 All of the following are associated with Goodpastures syndrome except _____. (Select all that apply.)
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.
1612 Individuals who have two defective alleles of the AIRE gene _____.
1613 All of the following autoimmune diseases are correctly matched with their HLA disease associations except _____.
1614 The haplotype A1B8DR3DQ2 is associated with several common autoimmune diseases including all of the following except _____.
1615 With the exception of ______, these autoimmune diseases are more prevalent in women than in men.
1616 Which of the following is not a characteristic of Graves disease?
1617 All of the following are true regarding thyroglobulin except _____.
1618 Which of the following describes myasthenia gravis?
1619 Which of the following is associated with antagonistic autoantibodies against cell-surface receptors or adhesion molecules? (Select all that apply.)
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 _____.
1621 The formation of ectopic lymphoid tissues occurs in all of the following conditions except _____.
1622 A(n) _____ binds to the antigen-binding site of another antibody.
1623 All of the following are linked to the development of rheumatoid arthritis or are associated with its treatment except _____. (Select all that apply.)
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.
e 04:08; acidic.
1625 Celiac disease exhibits all of the following symptoms except _____.
1626 All of the following are characteristics of tissue transglutaminase except ____.
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.)
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.
|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.
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.
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.)
1641 Chronic diseases in which the immune response is targeted toward autologous entities of ones body are known as _____.
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.)
1647 Thyroid-stimulating hormone is made in the _____ and induces the release of thyroid hormones after proteolytic processing of _____.
1648 Graves disease causes _____, whereas Hashimotos disease causes _____.
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.)
1652 Examples of rheumatic diseases caused by autoimmune responses include _____. (Select all that apply.)
1653 Another name for anti-immunoglobulin autoantibodies is _____.
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.
1655 Which of the following autoimmune diseases affect the nervous system? (Select all that apply.)
1656 _____ autoantibodies enhance receptor function.
1657 Antagonistic autoantibodies made against the insulin receptor cause _____. (Select all that apply.)
1658 Deficiency in the production of AIRE results in _____. (Select all that apply.)
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 _____.
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.
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.)
1664 Bacterial infections are associated with which of the following autoimmune diseases? (Select all that apply.)
1665 _____ is the term used to describe how pathogen antigens resemble host antigens and can sometimes trigger autoimmune disease.
1667 The upregulation of _____ by IFN- can contribute to antigen-specific T-cell activation on thyroid epithelium.
1668 A(n) _____ is an epitope that is typically not accessible to the immune system but is revealed under inflammatory or infectious states.
1669 The process by which the human thymus gradually decays is known as _____.
1670 The autoreactive CD4 T cells of elderly people with rheumatoid arthritis _____. (Select all that apply.)
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?
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?
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?
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?
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
1619 a, c, e
1623 e, j
(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
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
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.
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.
1640 a, c
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
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
1655 a, e
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.
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
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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