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USMLE® Step 1 > USMLE (S1) Immunology > Immunology - Immune Responses > Flashcards

Immunology - Immune Responses Flashcards

1
Q

Which cells secrete interleukin-1?

A

Macrophages

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2
Q

What are the effects of interleukin-1 secretion?

A

Acute inflammation; interleukin-1 induces recruitment of leukocytes, activates the endothelium to express adhesion molecules, and serves as an endogenous pyrogen

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3
Q

What are the effects of interleukin-2?

A

Interleukin-2 stimulates growth of helper and cytotoxic T cells

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4
Q

What are the functions of interleukin-3?

A

Growth and differentiation of stem cells in the bone marrow

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5
Q

Which cell type secretes interleukin-3?

A

Activated T cells

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6
Q

What are the functions of interleukin-4?

A

Promotion of B-cell growth and induction of class switching to immunoglobulin E and immunoglobulin G

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7
Q

What is the function of interleukin-5? By what type of cells is it secreted?

A

Interleukin-5 is involved in promotion of differentiation of B cells and induction of class switching to immunoglobulin A; it also stimulates production and activation of eosinophils; it is secreted by Th2 cells

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8
Q

What is the function of interleukin-6? By what cells is it produced?

A

Interleukin-6 stimulates production of acute-phase reactants and immunoglobulins; it is produced by helper T cells and macrophages

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9
Q

Which cytokine is a major chemotactic factor for neutrophils?

A

Interleukin-8

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10
Q

Which cell type secretes interleukin-8?

A

Macrophages

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11
Q

Which cytokine, released by regulatory T cells, inhibits actions of activated T cells?

A

Interleukin-10

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12
Q

What is the function of interleukin-12? Which cells secrete interleukin-12?

A

Interleukin-12 activates natural killer and Th1 cells; it is secreted by B cells and macrophages

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13
Q

What cytokine that is secreted by Th1 cells stimulates macrophages?

A

γ-Interferon

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14
Q

Which cytokine, secreted by macrophages, is an important mediator of septic shock?

A

Tumor necrosis factor

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15
Q

What are the effects of tumor necrosis factor secretion? By which cells is tumor necrosis factor secreted?

A

Tumor necrosis factor mediates leukocyte recruitment and vascular leak; it is secreted by macrophages

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16
Q

Which cytokine stimulates bone marrow?

A

Interleukin-3

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17
Q

Which cell surface proteins are found on helper T cells?

A

CD4, TCR, CD3, CD28, CD40L

CD28 provides co-stimulatory signals for T cell activation.

CD40L is important for communication with B cells and antigen-presenting cells.

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18
Q

Which cell surface proteins are found on cytotoxic T cells?

A

CD8, TCR, CD3

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19
Q

Which cell surface proteins are found on B cells?

A

IgM, CD19, CD20, CD21, CD40, MHCII, B7

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20
Q

Which cell surface proteins are found on macrophages?

A

MHCII, B7, CD40, CD14, receptors for Fc and C3b

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21
Q

Which cell surface proteins are found on natural killer cells?

A

Receptors for MHC I, CD16, CD56

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22
Q

True or False? All human cells have major histocompatibility complex I.

A

False; mature red blood cells do not have major histocompatibility complex I

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23
Q

Which two types of immunoglobulins activate complement via the classic pathway?

A

Immunoglobulin G and Immunoglobulin M

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24
Q

What triggers the activation of complement via the alternative pathway?

A

Microbial surfaces (especially endotoxin)

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25
Q

What triggers the activation of complement via the classic pathway?

A

Antigen-antibody complexes

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26
Q

What triggers the activation of complement via the lectin pathway?

A

Microbial surfaces

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27
Q

In the complement system, the plasma proteins C1, C2, C3, and C4 are important for the neutralization of what types of infectious agents?

A

Viruses

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28
Q

The membrane attack complex of complement is especially important in the defense against what type of bacteria?

A

Gram-negative bacteria

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29
Q

In the complement system, what is the function of the plasma protein C3b?

A

Opsonization

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30
Q

In the complement system, the activation of what two plasma proteins can cause anaphylaxis?

A

C3a and C5a

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31
Q

Which complement protein is responsible for neutrophil chemotaxis?

A

C5a

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32
Q

In the complement system, the membrane attack complex performs what function?

A

Cytolysis of target antigen

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33
Q

The membrane attack complex is composed of which complement proteins?

A

C5b, C6, C7, C8, and C9

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34
Q

The deficiency of what plasma protein leads to overactive complement and hereditary angioedema?

A

C1 esterase inhibitor

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35
Q

What are the clinical sequelae of hereditary complement C3 deficiency?

A

Recurrent pyogenic sinus and respiratory tract infections

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36
Q

In the complement system, the deficiency of which plasma proteins can predispose someone to Neisseria bacteremia?

A

C5-C8

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37
Q

In the complement system, the deficiency of which plasma protein leads to paroxysmal nocturnal hemoglobinuria?

A

Decay-accelerating factor also known as CD55.

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38
Q

True or False? Decay accelerating factor and C1 esterase inhibitor help prevent complement activation on host cells.

A

TRUE

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39
Q

In the complement system, the cleavage of which plasma protein is the first shared step for both the alternative and classic pathways?

A

C5

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40
Q

What is the name for the complex of MC5b, 6, 7, 8, and 9 in the final step of the complement system, which lyses target cells?

A

Membrane attack complex

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41
Q

What are the two primary opsonins used to defend against bacteria?

A

C3b and immunoglobulin G

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42
Q

Name the class of plasma proteins secreted to place uninfected cells in an antiviral state and that inhibit viral protein synthesis.

A

Interferons

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43
Q

Name three mechanisms by which interferons interfere with viral protein synthesis.

A

Interferons induce viral mRNA-destroying proteins, increase major histocompatibility complex I and II expression, and activate natural killer cells to kill virus-infected cells

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44
Q

Which interferons increase major histocompatibility complex I and II expression and antigen presentation in all cells?

A

γ-Interferon

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45
Q

Which interferons inhibit viral protein synthesis?

A

α-interferon and β-interferon induce production of ribonucleases that inhibit viral protein synthesis.

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46
Q

Which cytokines activate natural killer cells to kill virus-infected cells?

A

Interferons

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47
Q

Interferons activate _____ (natural killer cells/macrophages) to kill virus-infected cells.

A

Natural killer cells

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48
Q

How does active immunity differ from passive immunity?

A

In active immunity, the host forms antibodies; in passive immunity, the host receives preformed antibodies

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49
Q

Give four examples of diseases for which preformed antibodies are given after exposure.

A

Tetanus, botulism, hepatitis B, and rabies (remember: To Be Healed Rapidly)

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50
Q

What is the approximate half-life of antibodies transferred from one host to another in passive immunity?

A

3 weeks

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51
Q

Which antibody in breast milk confers passive immunity to newborns?

A

Immunoglobulin A

IgA is the main antibody that protects mucosal surfaces in newborns.

Passive immunity is temporary but crucial for early life protection.

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52
Q

Antigenic _____ (drift/shift) is the natural mutation over time of known strains of influenza to evade the immune system.

A

Drift; this is the source of the annual influenza epidemics

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53
Q

Antigenic _____ (drift/shift) is the process by which two strains of influenza combine to form a new subtype that has a mixture of the surface antigens of the two original strains.

A

Shift; this is the source of worldwide influenza pandemics such as the 2009 H1N1 flu

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54
Q

In what way does Salmonella bacteria exhibit antigenic variation?

A

Via flagellar variants

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55
Q

In what way does Neisseria gonorrhea exhibit antigenic variation?

A

Pilus protein variation

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56
Q

In what way does influenza demonstrate antigenic variation?

A

RNA shifts and drifts

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57
Q

In what way do trypanosomes demonstrate antigenic variation?

A

Programmed rearrangement

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58
Q

Describe the process of T-cell anergy.

A

Self-reactive T cells become nonreactive when they do not receive a costimulatory molecule

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59
Q

True or False? Both B cells and T cells can develop anergy to self-antigens, but B cells display more complete tolerance.

A

False; tolerance to self-antigens is greater in T cells than in B cells

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60
Q

List four bacterial infections that can cause granulomatous disease

A

Tuberculosis, syphilis, leprosy, and cat scratch fever

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61
Q

What are three noninfectious conditions associated with granulomatous disease?

A

Sarcoidosis, Crohn’s disease, berylliosis

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62
Q

Name the four cell types found in granulomas.

A

Epithelioid cells and giant cells are specialized macrophages; fibroblasts and lymphocytes are also found in granulomas

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63
Q

Which type of hypersensitivity reaction involves antigen cross-linking immunoglobulin E on mast cells and basophils, triggering the release of histamine?

A

Type I

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64
Q

Which type of hypersensitivity reaction develops rapidly after antigen exposure as a result of preformed antibody?

A

Type I

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65
Q

Which type of hypersensitivity reaction involves immunoglobulin M and immunoglobulin G binding to the body’s own cells, thereby leading to lysis by complement or phagocytosis?

A

Type II hypersensitivity reaction

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66
Q

Which type of hypersensitivity reaction causes fever, urticaria, arthralgias, proteinuria, and lymphadenopathy 5 to 10 days after antigen exposure?

A

Serum sickness (a type III hypersensitivity reaction)

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67
Q

Which type of hypersensitivity reaction is caused by immune complexes that activate complement and attract neutrophils that release lysosomal enzymes?

A

Type III

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68
Q

Which type of hypersensitivity reaction is the Arthus reaction?

A

Type III

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69
Q

What is the Arthus reaction?

A

A reaction caused when intradermal injection of an antigen leads to tissue edema and necrosis due to immune complex formation and complement activation (type III hypersensitivity reaction)

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70
Q

What is serum sickness?

A

An immune complex disease (type III hypersensitivity) in which antibodies to foreign proteins are produced and deposited in tissues where they fix complement and lead to tissue damage

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71
Q

What are the signs and symptoms of serum sickness?

A

Fever, urticaria, arthralgias, proteinuria and lymphadenopathy

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72
Q

How long does it take after exposure to antigen for the fever, urticaria, and arthralgias characteristic of serum sickness to develop?

A

5-10 days

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73
Q

What is the cause of most cases of serum sickness?

A

Drugs

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74
Q

What two components make up the immune complexes that cause type III hypersensitivity reactions?

A

Antigens and antibodies; antigen-antibody complexes activate complement to cause tissue damage

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75
Q

What type III sensitivity reaction is characterized by local edema, necrosis, and the activation of complement?

A

Arthus reaction

76
Q

Which type of hypersensitivity reaction is mediated by T cells?

A

Type IV hypersensitivity reaction

77
Q

What cellular processes underlie a type IV hypersensitivity reaction?

A

Sensitized T cells encounter antigen and then release lymphokines that lead to macrophage activation

78
Q

How does the mnemonic ACID help one remember important features of the four different types of hypersensitivity reactions?

A

Type I: Anaphylactic and Atopic; type II: Cytotoxic (antibody mediated); type III: Immune complex; and type IV: Delayed (cell mediated)

79
Q

What three mechanisms are involved in the tissue damage of antibody-mediated (type II) hypersensitivity reactions?

A
  1. Opsonization/activation of complement;
  2. antibody recruitment of neutrophils and macrophages leading to tissue damage;
  3. antibody binding to normal cells and interfering with function
80
Q

Which two tests can evaluate whether a type II hypersensitivity reaction is causing hemolysis?

A

Direct and indirect Coombs tests

81
Q

Which type of hypersensitivity reaction is provoked by a PPD injection?

A

Type IV

82
Q

What are the 4 Ts associated with type IV hypersensitivity reactions?

A

T lymphocyte-mediated, Transplant rejection, TB skin tests, and Touching (contact dermatitis)

83
Q

Which type of hypersensitivity reaction includes contact dermatitis?

A

Type IV

84
Q

Which type of hypersensitivity reaction is anaphylaxis?

A

Type I

85
Q

Which type of hypersensitivity reaction is allergic rhinitis?

A

Type I

86
Q

Hemolytic anemia is a type _____ hypersensitivity reaction.

A

Type II

87
Q

Which type of hypersensitivity reaction is pernicious anemia?

A

Type II

88
Q

Idiopathic thrombocytopenic purpura is a type ____ hypersensitivity reaction.

A

Type II

89
Q

Which type of hypersensitivity reaction is erythroblastosis fetalis?

A

Type II

90
Q

Which type of hypersensitivity reaction describes rheumatic fever?

A

Type II

91
Q

Goodpasture’s syndrome is caused by which type of hypersensitivity reaction?

A

Type II hypersensitivity reaction

92
Q

Which type of hypersensitivity reaction causes the skin conditions bullous pemphigoid and pemphigus vulgaris?

A

Type II

93
Q

Which type of hypersensitivity reaction is Graves’ disease?

A

Type II; Graves’ disease is a special case because the antibodies involved cause cell activation (thyroid hormone secretion) rather than tissue damage

94
Q

Myasthenia gravis is a type _____ hypersensitivity reaction.

A

Type II

95
Q

Which type of hypersensitivity reaction causes systemic lupus erythematosus?

A

Type III

96
Q

Rheumatoid arthritis is a type _____ hypersensitivity reaction.

A

Type III; in the case of rheumatoid arthritis, the body’s own antibodies are the antigens to which the immune system reacts and forms immune complexes

97
Q

Polyarteritis nodosa is a type _____ hypersensitivity reaction.

A

Type III

98
Q

What type of hypersensitivity reaction causes poststreptococcal glomerulonephritis?

A

Type III hypersensitivity reaction

99
Q

Swelling and inflammation following a tetanus vaccine represents the _____ _____, a type _____ hypersensitivity reaction.

A

Arthus reaction; type III

100
Q

Hypersensitivity pneumonitis is a type _____ hypersensitivity reaction.

A

Type III

101
Q

What type of hypersensitivity reaction causes Hashimoto’s thyroiditis?

A

T-cell-mediated type IV reaction

102
Q

Which type of hypersensitivity reaction is type 1 diabetes mellitus?

A

Type IV

103
Q

Multiple sclerosis is mediated by _____ (B/T) cells.

A

T cells; multiple sclerosis involves a type IV hypersensitivity reaction

104
Q

Placement of a PPD test elicits which hypersensitivity reaction?

A

Type IV

105
Q

True or False? Graft-versus-host disease and hyperacute transplant rejection are both antibody-mediated.

A

False: Graft-versus-host disease is a T-cell mediated hypersensitivity reaction (type IV); hyperacute transplant rejection is antibody-mediated, but is not a hypersensitivity reaction

106
Q

Guillain-Barr syndrome is a type _____ hypersensitivity reaction.

A

Type IV

107
Q

What disorder is most commonly associated with antinuclear antibodies?

A

Systemic lupus erythematosus (although antinuclear antibodies are nonspecific)

108
Q

What disorder is most commonly associated with anti-double stranded DNA and anti-Smith autoantibodies?

A

Systemic lupus erythematosus (more specific than antinuclear antibodies)

109
Q

What disorder is most commonly associated with antihistone autoantibodies?

A

Drug-induced lupus

110
Q

What disorder is most commonly associated with anti-immunoglobulin G autoantibodies?

A

Rheumatoid arthritis (anti-immunoglobulin G antibodies are also known as rheumatoid factor)

111
Q

What family of disorders is most commonly associated with anti-neutrophil (C-ANCA, P-ANCA) autoantibodies?

A

Vasculitides

112
Q

What disorder is most commonly associated with anticentromere autoantibodies?

A

Scleroderma (CREST syndrome)

113
Q

What disorder is most commonly associated with anti-Scl-70 (anti-DNA topoisomerase I) autoantibodies?

A

Scleroderma (diffuse)

114
Q

What disorder is most commonly associated with antimitochondrial autoantibodies?

A

Primary biliary cirrhosis

115
Q

What disorder is most commonly associated with antigliadin and antiendomysial autoantibodies?

A

Celiac disease

116
Q

What disorder is most commonly associated with anti-basement membrane autoantibodies?

A

Goodpasture’s syndrome

117
Q

What disorder is most commonly associated with antidesmoglein cell autoantibodies?

A

Pemphigus vulgaris

118
Q

What disorder is most commonly associated with antimicrosomal autoantibodies?

A

Hashimoto’s thyroiditis

119
Q

What autoantibodies are associated with Hashimoto’s thyroiditis?

A

Antimicrosomal and anti-thyroglobulin autoantibodies

120
Q

What disorder is most commonly associated with anti-Jo-1 autoantibodies?

A

Polymyositis or dermatomyositis

121
Q

Which two autoantibodies should be tested for if Sjögren’s syndrome is suspected?

A

Anti-SS-A (anti-Ro) and anti-SS-B (anti-La)

122
Q

Mixed connective tissue disease can be associated with which autoantibodies?

A

Anti-U1 ribonucleoprotein

123
Q

If autoimmune hepatitis is suspected, which autoantibodies should be tested?

A

Anti-smooth muscle antibodies

124
Q

Anti-glutamate decarboxylase antibodies are most commonly associated with which autoimmune disease?

A

Type 1 diabetes mellitus

125
Q

Wegener’s granulomatosis is a vasculitis associated with what autoantibody?

A

c-ANCA

126
Q

What X-linked recessive genetic defect is associated with low levels of all classes of immunoglobulins and is caused by a defective tyrosine kinase gene?

A

Bruton’s agammaglobulinemia

127
Q

Which X-linked recessive genetic defect is associated with recurrent bacterial infections after 6 months of age, when levels of maternal immunoglobulin G antibody decline?

A

Bruton’s agammaglobulinemia

128
Q

Name the immune deficiency in which the thymus and parathyroids fail to develop.

A

DiGeorge’s syndrome (thymic aplasia)

129
Q

Which immune deficiency is caused by failure of the third and fourth pharyngeal pouches to develop?

A

DiGeorge’s syndrome (thymic aplasia)

130
Q

What are the clinical manifestations of DiGeorge’s syndrome?

A

Tetany as a result of hypocalcemia and recurrent viral and fungal infections caused by a T-cell deficiency

131
Q

What is the inheritence pattern of Bruton’s agammaglobulinemia?

A

X-linked recessive

132
Q

What immune deficiency is associated with congenital defects of the heart and great vessels and with 22q11 deletion?

A

DiGeorge’s syndrome (thymic aplasia)

133
Q

Which cell line is diminished in thymic aplasia?

A

T cells

134
Q

Which cell line is diminished in Bruton’s agammaglobulinemia?

A

B cells

135
Q

Is severe combined immunodeficiency characterized by the diminished production of B cells, T cells, or both B and T cells?

A

Both B and T cells

136
Q

Which immune deficiency is caused by the decreased activation of T cells and results in patients presenting with disseminated mycobacterial infections?

A

Interleukin-12 receptor deficiency

137
Q

Which immune deficiency is caused by a defect in the CD40 ligand on CD4 helper T cells that results in an inability to switch antibody classes?

A

Hyper-IgM syndrome; B-cells can produce immunoglobulin M without class switching

138
Q

Which immune deficiency presents early in life with severe pyogenic infections and affects patients with high serum levels of immunoglobulin M and low levels of immunoglobulins G, A, and E?

A

Hyper-IgM syndrome

139
Q

Which immune deficiency is caused by a failure of γ-interferon production by helper T cells that results in neutrophils failing to respond to chemotactic stimuli?

A

Job’s syndrome

140
Q

List the symptoms of Job’s syndrome; use the mnemonic FATED

A

Coarse Facies; noninflamed staphylococcal Abscesses, retained primary Teeth, increased immunoglobulin E levels, and Dermatologic problems

141
Q

Does interleukin-12 receptor deficiency result in the diminished activation of B cells, T cells, or macrophages?

A

T cells lacking the receptor are not activated by interleukin-12; as a result they do not produce interferon-γ to activate macrophages

142
Q

Is hyper-IgM syndrome characterized by the diminished activation of B cells, T cells, or macrophages?

A

B cells are unable to switch antibody classes due to absent CD40 signaling

143
Q

Is Job’s syndrome characterized by the diminished activation of B cells, T cells, or neutrophils?

A

Neutrophils fail to respond to chemotactic stimuli due to a failure of interferon-γ production

144
Q

Which immune deficiency presents early in life with severe pyogenic and fungal infections and delayed separation of the umbilicus?

A

Leukocyte adhesion deficiency syndrome

145
Q

Which immune deficiency involves patients presenting with recurrent skin and mucous membrane Candida infections?

A

Chronic mucocutaneous candidiasis

146
Q

Which immune cells are dysfunctional in chronic mucocutaneous candidiasis?

A

T cells

147
Q

Which immune deficiency involves patients presenting with recurrent sinus and lung infections, milk allergies, and diarrhea?

A

Selective immunoglobulin A deficiency

148
Q

What is the most common selective immunoglobulin deficiency?

A

Selective immunoglobulin A deficiency

149
Q

Which immune deficiency disease presents with normal numbers of circulating B cells but a decreased number of plasma cells?

A

Common variable immunodeficiency

150
Q

Patients with common variable immunodeficiency have an increased risk of which two noninfectious conditions?

A

Autoimmune disease and lymphoma

151
Q

Which disease, caused by defective DNA repair, presents with visible dilated capillaries in the skin, cerebellar dysfunction, and immunoglobulin A deficiency?

A

Ataxia-telangiectasia

152
Q

What X-linked immune deficiency is associated with elevated immunoglobulin A levels, normal immunoglobulin E levels, and low immunoglobulin M levels?

A

Wiskott-Aldrich syndrome

153
Q

Which immune deficiency presents with a triad of symptoms that includes recurrent pyogenic infections, thrombocytopenic purpura, and eczema?

A

Wiskott-Aldrich syndrome

154
Q

Which autosomal-recessive immune deficiency presents with recurrent pyogenic staph and strep infections, partial albinism, and peripheral neuropathy?

A

Chdiak-Higashi disease

155
Q

Which autosomal-recessive immune deficiency is caused by defective microtubular function causing impaired phagocytosis?

A

Chdiak-Higashi disease

156
Q

Which immune deficiency is caused by a defect in microbicidal capability of neutrophils resulting from a lack of NADPH oxidase?

A

Chronic granulomatous disease

157
Q

The presence of which immune deficiency is confirmed with a negative nitroblue tetrazolium dye reduction test?

A

Chronic granulomatous disease

158
Q

Which immune deficiency involves patients presenting with marked susceptibility to opportunistic infections with Staphylococcus aureus, Escherichia coli, and Aspergillus?

A

Chronic granulomatous disease; organisms that produce catalase resist neutrophil killing in this disease

159
Q

What are three possible causes of severe combined immunodeficiency?

A

Failure to synthesize major histocompatibility complex II antigens, defective interleukin-2 receptors, or adenosine deaminase deficiency

160
Q

Which immune deficiency results from a defect in LFA-1 (or CD18) on phagocytes?

A

Leukocyte adhesion deficiency syndrome

161
Q

Which immune deficiency can result from a defect in stem cell differentiation and involves patients presenting with recurrent viral, bacterial, fungal, and protozoal infections?

A

Severe combined immunodeficiency; adenosine deaminase deficiency causes a failure of immune cell precursor maturation

162
Q

Pro-T cells cannot mature when lacking which receptor?

A

Interleukin-2 receptor; a faulty receptor results in severe combined immunodeficiency

163
Q

In DiGeorge syndrome _____ cannot fully mature.

A

Immature T cells

164
Q

Severe combined immunodeficiency due to major histocompatibility complex II deficiency causes dysfunction of which immune cells?

A

CD4 T cells

165
Q

Bruton’s agammaglobulinemia affects B-cell maturation at which point in development?

A

In Bruton’s, pre-B cells do not become immature B cells

166
Q

Hyper-IgM syndrome results in a deficiency of which antibodies?

A

Immunoglobulin G, immunoglobulin A and immunoglobulin E; due to failure of class-switching

167
Q

Which immune deficiency completely blocks further development of lymphoid stem cells?

A

Severe combined immunodeficiency due to adenosine deaminase deficiency

168
Q

What disease results from an inability of B cells to become antibody-secreting plasma cells?

A

Common variable immunodeficiency

169
Q

True or False? An autograft signifies that donor and recipient are the same person.

A

TRUE

170
Q

A graft from an identical twin or clone is known as a ___ graft.

A

Syngeneic

171
Q

An allograft is a graft taken from a non-identical individual from the _____ (same/different) species.

A

Same

172
Q

A graft taken from a different species is known as a _______.

A

Xenograft

173
Q

What is the cause of hyperacute rejection?

A

Preformed antidonor antibodies in the transplant recipient

174
Q

True or False? In hyperacute rejection, the rejection of a donor organ occurs hours to days after transplantation.

A

False; rejection occurs within minutes as a result of the presence of preformed antidonor antibodies in the transplant recipient

175
Q

What type of transplant rejection is cell mediated as a result of cytotoxic T cells reacting against foreign major histocompatibility complexes?

A

Acute rejection

176
Q

How long after transplantation do patients develop symptoms of acute rejection? How can acute rejection be reversed?

A

Acute rejection occurs within weeks of transplantation; it can be reversed with immunosuppressants such as cyclosporine and muromonab-CD3 (OKT3)

177
Q

True or False? Acute rejection can be reversed with immunosuppressants such as cyclosporine and muromonab-CD3 (OKT3).

A

TRUE

178
Q

What process mediates chronic transplant rejection, and how can it be reversed?

A

Chronic rejection is caused by antibody- and T-cell-mediated vascular damage; it is irreversible

179
Q

Which type of transplant rejection is caused by antibody- and T-cell-mediated vascular damage?

A

Chronic rejection

180
Q

In chronic rejection of a transplant, vascular damage is mediated by _____ and _____.

A

Antibodies and T cells

181
Q

What is the vascular damage in chronic rejection of a transplant called?

A

Obliterative vascular fibrosis

182
Q

How long after transplantation do patients develop symptoms of chronic rejection?

A

Chronic rejection occurs over a period of months or years

183
Q

What is the mechanism of graft-versus-host disease?

A

Grafted immunocompetent T cells proliferate in the immunocompromised host and reject cells with foreign proteins, resulting in host organ dysfunction

184
Q

An organ transplant patient with a maculopapular rash, jaundice, hepatosplenomegaly, and diarrhea may be suffering from what disease?

A

Graft-versus-host disease

185
Q

True or False? Hyperacute, acute, and chronic transplant rejection are antibody-mediated processes.

A

False; only hyperacute and chronic transplant rejection are mediated by antibodies; acute rejection is cell mediated via cytotoxic T cells reacting against foreign major histocompatibility complexes

USMLE (S1) Immunology (4 decks)

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