Unit 6: Hypersensitivity; Transplantation; Autoimmunity - Practice Quiz

BTS511 — Immunology 60 Questions
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1 Which antibody class primarily mediates type I hypersensitivity reactions?

type I hypersensitivity Easy
A. IgA
B. IgM
C. IgG
D. IgE

2 Which cell releases histamine during a type I hypersensitivity reaction?

type I hypersensitivity Easy
A. Neutrophil
B. Mast cell
C. Plasma cell
D. Cytotoxic T cell

3 Which of the following is a classic example of a type I hypersensitivity reaction?

type I hypersensitivity Easy
A. Hemolytic disease of the newborn
B. Anaphylaxis
C. Serum sickness
D. Contact dermatitis

4 Type II hypersensitivity reactions are primarily mediated by antibodies directed against:

type II hypersensitivity Easy
A. Sensitized T lymphocytes
B. Cell surface or tissue antigens
C. IgE-bound allergens
D. Soluble circulating antigens

5 Which condition is a typical example of type II hypersensitivity?

type II hypersensitivity Easy
A. Arthus reaction
B. Hay fever
C. ABO blood transfusion reaction
D. Poison ivy dermatitis

6 Which antibody classes are mainly involved in type II hypersensitivity?

type II hypersensitivity Easy
A. IgA and IgE
B. IgG and IgM
C. IgE and IgD
D. IgD and IgM

7 Type III hypersensitivity reactions are caused by the deposition of:

type III hypersensitivity Easy
A. Autoreactive B cells
B. Free IgE molecules
C. Sensitized T cells
D. Antigen-antibody immune complexes

8 Which of the following is a classic example of type III hypersensitivity?

type III hypersensitivity Easy
A. Tuberculin skin test
B. Anaphylactic shock
C. Serum sickness
D. Graves' disease

9 The localized inflammatory response caused by immune complex deposition at a site of antigen injection is called the:

type III hypersensitivity Easy
A. Arthus reaction
B. Prausnitz-Küstner reaction
C. Shwartzman reaction
D. Wheal-and-flare reaction

10 Type IV hypersensitivity is also known as:

type IV hypersensitivity Easy
A. Immune complex hypersensitivity
B. Immediate hypersensitivity
C. Cytotoxic hypersensitivity
D. Delayed-type hypersensitivity

11 Which cells mediate type IV hypersensitivity reactions?

type IV hypersensitivity Easy
A. Platelets
B. B lymphocytes
C. Mast cells
D. T lymphocytes

12 The tuberculin (Mantoux) skin test is an example of which type of hypersensitivity?

type IV hypersensitivity Easy
A. Type IV
B. Type III
C. Type I
D. Type II

13 The main antigens responsible for graft rejection between individuals are the:

immunologic basis of graft rejection Easy
A. Major histocompatibility complex (MHC) antigens
B. Rh factor antigens
C. Heat shock proteins
D. ABO blood group antigens only

14 A graft transferred between genetically identical individuals is called a(n):

immunologic basis of graft rejection Easy
A. Isograft
B. Xenograft
C. Autograft
D. Allograft

15 A graft between two different species is termed a:

immunologic basis of graft rejection Easy
A. Allograft
B. Xenograft
C. Isograft
D. Autograft

16 Tissue typing before transplantation is primarily performed to match:

tissue typing Easy
A. Blood glucose levels
B. Enzyme concentrations
C. HLA antigens
D. Body temperature

17 In which structure of the human genome are HLA genes located?

tissue typing Easy
A. Chromosome 6
B. Chromosome 14
C. Chromosome 21
D. Chromosome 1

18 Which type of T cell is the main effector in cell-mediated graft rejection?

cell mediated graft rejection Easy
A. Plasma cells
B. Natural killer T cells only
C. Regulatory T cells
D. Cytotoxic T cells

19 Which type of graft rejection typically occurs days to weeks after transplantation and is mainly cell-mediated?

cell mediated graft rejection Easy
A. Acute rejection
B. Chronic rejection
C. Latent rejection
D. Hyperacute rejection

20 Hyperacute graft rejection typically occurs:

clinical manifestations of graft rejection Easy
A. Only after immunosuppression stops
B. Within minutes to hours of transplantation
C. Several weeks after transplantation
D. Months to years after transplantation

21 A patient develops wheezing, urticaria, and hypotension within minutes of a bee sting. Which mediator released from mast cells is primarily responsible for the immediate vascular changes seen in this reaction?

type I hypersensitivity Medium
A. Lysozyme
B. Interferon-gamma
C. Histamine
D. Complement C3b

22 The late-phase reaction of type I hypersensitivity, occurring several hours after allergen exposure, is characterized by tissue infiltration primarily of which cell type?

type I hypersensitivity Medium
A. Cytotoxic T cells
B. Eosinophils
C. Plasma cells
D. Erythrocytes

23 A newborn develops hemolytic disease due to maternal anti-Rh antibodies. This condition is best classified as which type of hypersensitivity?

type II hypersensitivity Medium
A. Type IV (cell-mediated)
B. Type III (immune complex)
C. Type II (antibody-mediated cytotoxicity)
D. Type I (IgE-mediated)

24 In Graves' disease, autoantibodies bind the TSH receptor and stimulate thyroid hormone production. This is considered an atypical type II reaction because the antibodies:

type II hypersensitivity Medium
A. Alter receptor function rather than destroy cells
B. Trigger IgE-mediated degranulation
C. Form circulating immune complexes
D. Activate cytotoxic T lymphocytes

25 A patient develops fever, arthralgia, and proteinuria about 10 days after receiving antivenom serum. The renal damage is most likely caused by:

type III hypersensitivity Medium
A. Autoantibodies against the TSH receptor
B. Deposition of antigen-antibody complexes in glomeruli
C. Direct T-cell attack on tubular epithelium
D. IgE binding to mast cells in the kidney

26 Which feature distinguishes the Arthus reaction from anaphylaxis?

type III hypersensitivity Medium
A. It occurs within seconds of exposure
B. It is a localized immune-complex reaction at the injection site
C. It is mediated by IgE antibodies
D. It is caused by cytotoxic T cells

27 A positive tuberculin (Mantoux) skin test produces induration peaking at 48–72 hours. This delayed response is mediated primarily by:

type IV hypersensitivity Medium
A. Complement-fixing IgM antibodies
B. IgE-coated mast cells
C. Sensitized CD4+ T cells and macrophages
D. Circulating immune complexes

28 Contact dermatitis from nickel jewelry is a type IV reaction. The nickel ions act as haptens by:

type IV hypersensitivity Medium
A. Directly cross-linking IgE on mast cells
B. Forming soluble immune complexes in serum
C. Binding self proteins to become immunogenic
D. Activating complement via the classical pathway

29 A graft transplanted between genetically identical twins is generally accepted without rejection. This type of graft is called a:

immunologic basis of graft rejection Medium
A. Autograft
B. Xenograft
C. Allograft
D. Isograft (syngeneic graft)

30 Which molecules are the principal targets recognized by the recipient's T cells during allograft rejection?

immunologic basis of graft rejection Medium
A. MHC (HLA) molecules
B. Complement regulatory proteins
C. Immunoglobulin isotypes
D. ABO blood group enzymes

31 In direct allorecognition, recipient T cells recognize:

immunologic basis of graft rejection Medium
A. Donor peptides presented by recipient MHC
B. Free circulating donor antibodies
C. Intact donor MHC molecules on donor antigen-presenting cells
D. Complement fragments deposited on the graft

32 Before a kidney transplant, a crossmatch test is performed by mixing recipient serum with donor lymphocytes. A positive crossmatch indicates:

tissue typing Medium
A. Complete HLA identity between donor and recipient
B. Successful induction of graft tolerance
C. Preformed recipient antibodies against donor antigens
D. Absence of any immune response to the graft

33 Which HLA loci are considered most important to match for improving solid organ graft survival?

tissue typing Medium
A. Only HLA-C
B. ABO antigens alone
C. HLA-A, HLA-B, and HLA-DR
D. HLA-E, HLA-F, and HLA-G

34 Acute cellular rejection of a transplanted organ is primarily mediated by which effector cells?

cell mediated graft rejection Medium
A. Plasma cells secreting IgE
B. Neutrophils via immune complexes
C. CD8+ cytotoxic T lymphocytes
D. Eosinophils

35 Cyclosporine and tacrolimus prevent cell-mediated graft rejection mainly by:

cell mediated graft rejection Medium
A. Depleting all circulating B cells
B. Neutralizing complement in serum
C. Blocking IgE binding to mast cells
D. Inhibiting calcineurin and blocking IL-2 production

36 A transplanted kidney turns cyanotic and mottled within minutes of vascular anastomosis. This hyperacute rejection is caused by:

clinical manifestations of graft rejection Medium
A. Preformed antibodies activating complement in graft vessels
B. Delayed macrophage infiltration
C. Chronic fibrosis of graft vasculature
D. Slowly developing cytotoxic T-cell responses

37 Chronic graft rejection typically presents months to years after transplantation and is characterized histologically by:

clinical manifestations of graft rejection Medium
A. Immediate complement-mediated hemolysis
B. Vascular fibrosis and progressive luminal narrowing
C. Rapid vascular thrombosis within minutes
D. Dense neutrophil infiltration within hours

38 Which mechanism best explains how molecular mimicry contributes to autoimmune disease?

introduction to autoimmune disorders Medium
A. T cells lose their T-cell receptors entirely
B. Microbial antigens resemble self antigens, cross-activating autoreactive lymphocytes
C. IgE antibodies are produced against all self tissues
D. Complement proteins directly mutate into autoantigens

39 In Hashimoto's thyroiditis, hypothyroidism results primarily from:

organ specific autoimmune disease Medium
A. IgE-mediated mast cell degranulation in the thyroid
B. T-cell and antibody-mediated destruction of thyroid follicular cells
C. Immune complex deposition in the thyroid vasculature
D. Stimulating antibodies overactivating the TSH receptor

40 Systemic lupus erythematosus (SLE) is characterized by antibodies against nuclear components and tissue injury mediated largely by:

systemic autoimmune disease Medium
A. IgE-mediated anaphylaxis
B. Hyperacute complement activation within minutes
C. Direct cytotoxic destruction of neurons only
D. Immune complex deposition (type III mechanism)

41 A patient develops anaphylaxis within minutes of a bee sting. During the late-phase reaction (6–12 hours later), tissue biopsy shows a predominant cellular infiltrate. Which cell type and mediator combination is MOST characteristic of this late phase rather than the immediate phase?

type I hypersensitivity Hard
A. Basophils releasing preformed tryptase
B. Eosinophils recruited by IL-5 and eotaxin
C. Neutrophils driven by C5a alone
D. Mast cells releasing preformed histamine

42 A researcher measures a patient's total serum IgE and finds it normal, yet the patient has a strongly positive skin prick test and clinical allergy to peanut. What is the BEST explanation for allergy despite normal total IgE?

type I hypersensitivity Hard
A. Normal total IgE excludes any type I reaction
B. Allergen-specific IgE can be elevated even when total IgE is within normal range
C. Skin prick tests measure IgG rather than IgE
D. Total IgE always predicts clinical severity accurately

43 In Goodpasture syndrome, autoantibodies target the non-collagenous (NC1) domain of the chain of type IV collagen. Why are the kidney and lung selectively affected in this disease?

type II hypersensitivity Hard
A. Both organs express the chain of type IV collagen in their basement membranes
B. Both organs harbor resident autoreactive B cells only
C. Both organs uniquely lack complement regulatory proteins
D. Both organs have fenestrated endothelium allowing IgE entry

44 A newborn of a group O mother develops mild hemolytic disease, while a different group A infant of an Rh-negative mother sensitized in a prior pregnancy develops severe disease. Which statement BEST explains the difference in severity between ABO and Rh hemolytic disease of the newborn?

type II hypersensitivity Hard
A. Rh antigens are poorly expressed on fetal red cells
B. Anti-Rh (D) is mainly IgG which crosses the placenta, whereas natural anti-A/B is largely IgM
C. Anti-A/B antibodies are exclusively IgG and cross the placenta more efficiently
D. ABO incompatibility requires prior sensitization like Rh does

45 In an Arthus reaction, a patient injected intradermally with antigen develops localized edema, hemorrhage, and necrosis over several hours. What is the KEY pathogenic event distinguishing this from a type I reaction at the same site?

type III hypersensitivity Hard
A. Antigen-specific CD8 T cell cytotoxicity of keratinocytes
B. Local immune complex deposition activating complement and neutrophil influx
C. Mast cell degranulation triggered by cross-linked IgE
D. Direct antibody binding to cell surface antigens causing lysis

46 The size and solubility of immune complexes influence their pathogenicity. Which type of immune complex is MOST likely to deposit in tissues and cause type III disease?

type III hypersensitivity Hard
A. Very large insoluble complexes formed in extreme antibody excess
B. Monomeric antibody bound to a single soluble antigen
C. Small-to-intermediate soluble complexes formed near antigen excess
D. Complexes composed exclusively of IgE and antigen

47 A tuberculin skin test is read at 48–72 hours as an area of induration. Which mechanism explains why the peak response is delayed rather than immediate?

type IV hypersensitivity Hard
A. Circulating IgG must first form immune complexes at the site
B. Time is required for antigen presentation and clonal recruitment of sensitized Th1 cells and macrophages
C. Mast cells must synthesize new leukotrienes de novo
D. Complement components require 48 hours to assemble on membranes

48 In contact dermatitis to nickel, the metal itself is too small to be immunogenic. What immunological concept explains how nickel triggers a type IV response?

type IV hypersensitivity Hard
A. Nickel forms soluble immune complexes deposited in the dermis
B. Nickel directly cross-links IgE on Langerhans cells
C. Nickel acts as a hapten binding self-proteins to form a complete antigen
D. Nickel is a superantigen activating all T cells nonspecifically

49 Hyperacute rejection of a transplanted kidney occurs within minutes of vascular anastomosis. Which pre-existing immunological factor is MOST responsible?

immunologic basis of graft rejection Hard
A. Recipient macrophages responding to ischemia-reperfusion injury
B. Naive recipient T cells recognizing donor MHC via direct presentation
C. De novo alloantibody produced after grafting
D. Preformed recipient antibodies against donor HLA or ABO antigens

50 A recipient's T cells can recognize donor alloantigen via two pathways. Which statement correctly contrasts direct versus indirect allorecognition?

immunologic basis of graft rejection Hard
A. Direct: recipient T cells recognize intact donor MHC on donor APCs; indirect: recipient T cells recognize donor peptides on recipient MHC
B. Direct: recipient T cells recognize donor peptides on recipient APCs; indirect: recognition of intact donor MHC
C. Direct recognition is the dominant driver of chronic late rejection
D. Both pathways require processing of donor MHC by recipient APCs

51 A patient awaiting a kidney transplant has a high panel reactive antibody (PRA) of 85%. What does this value indicate for transplant planning?

tissue typing Hard
A. The recipient's own HLA is unusually rare in the population
B. The recipient is broadly sensitized and will be incompatible with most potential donors
C. The recipient has strong T cell immunity to most donors
D. The recipient will require no crossmatch before transplant

52 A complement-dependent cytotoxicity (CDC) crossmatch is positive between donor lymphocytes and recipient serum. What is the correct interpretation and consequence?

tissue typing Hard
A. Recipient has antibodies against donor HLA; transplant is contraindicated due to hyperacute rejection risk
B. Recipient lacks anti-donor antibodies; transplant can proceed safely
C. Donor and recipient are HLA-identical and ideal for transplant
D. Result indicates only T cell mismatch requiring more immunosuppression

53 In acute cellular rejection of a solid organ graft, which effector mechanism causes direct parenchymal cell destruction?

cell mediated graft rejection Hard
A. CD8 cytotoxic T lymphocytes recognizing donor MHC class I and inducing apoptosis
B. B cells directly phagocytosing donor epithelial cells
C. IgE-mediated mast cell degranulation on graft endothelium
D. Neutrophils releasing preformed histamine into the interstitium

54 Calcineurin inhibitors such as cyclosporine and tacrolimus are used to prevent cellular rejection. What is their primary molecular mechanism?

cell mediated graft rejection Hard
A. Inhibiting complement C3 convertase formation
B. Depleting circulating B cells via CD20 targeting
C. Directly lysing activated cytotoxic T lymphocytes
D. Blocking calcineurin-dependent NFAT activation and thereby IL-2 transcription in T cells

55 A kidney transplant recipient presents 8 months post-transplant with gradually rising creatinine, proteinuria, and biopsy showing interstitial fibrosis, tubular atrophy, and vascular intimal thickening. Which type of rejection is MOST consistent with these findings?

clinical manifestations of graft rejection Hard
A. Acute cellular rejection
B. Accelerated rejection
C. Chronic rejection
D. Hyperacute rejection

56 In graft-versus-host disease (GVHD) following allogeneic bone marrow transplant, which triad of organs is classically involved and why does this reaction occur?

clinical manifestations of graft rejection Hard
A. Skin, liver, and gut, because donor T cells attack recipient tissues
B. Kidney, lung, and heart, because recipient antibodies attack the graft
C. Brain, spleen, and pancreas, due to recipient CTL activity
D. Bone, joints, and muscle, because of complement deposition

57 Central and peripheral tolerance mechanisms normally prevent autoimmunity. A mutation in the AIRE gene causes APECED/APS-1. What is the underlying defect?

introduction to autoimmune disorders Hard
A. Impaired expression of tissue-specific self-antigens in the thymus, allowing autoreactive T cells to escape negative selection
B. Excessive complement activation destroying self-tolerant cells
C. Failure of B cell receptor editing in the bone marrow
D. Overactivation of regulatory T cells suppressing all immunity

58 Molecular mimicry is proposed as a mechanism triggering autoimmunity after infection. Which example BEST illustrates this concept?

introduction to autoimmune disorders Hard
A. Contact dermatitis, where nickel haptens modify self-proteins
B. Serum sickness, where immune complexes deposit in joints
C. Anaphylaxis, where IgE binds a food allergen
D. Rheumatic fever, where antibodies to streptococcal M protein cross-react with cardiac myosin

59 In Graves disease, hyperthyroidism results despite low circulating TSH. What is the immunologic mechanism producing this paradox?

organ specific autoimmune disease Hard
A. Stimulatory autoantibodies bind and activate the TSH receptor, driving thyroid hormone output independent of pituitary TSH
B. Autoantibodies to thyroglobulin directly stimulate hormone synthesis
C. Immune complexes block iodine uptake, lowering TSH
D. Cytotoxic T cells destroy thyroid follicular cells, releasing stored hormone

60 A young woman with SLE develops glomerulonephritis. Serology shows high anti-dsDNA titers and low serum C3 and C4. What best explains the low complement levels?

systemic autoimmune disease Hard
A. Overproduction of complement inhibitors by hepatocytes
B. Genetic deficiency of complement synthesis unrelated to disease activity
C. Consumption of complement by immune complex deposition and activation in tissues
D. Increased complement inactivation by regulatory T cells