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Immunology COM > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Which of the hypersensitivity reactions is cell mediated?

A

Type IV

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2
Q

What antibody mediates type I reactions?

A

IgE

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3
Q

What antibodies mediate types II and III reactions?

A

IgG and IgM

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4
Q

What are type I reactions also referred to as?

A

Allergic reaction, immediate hypersensitivity, or anaphylactic hypersensitivity

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5
Q

In type I reactions, allergens (ie, antigens) are presented to Th2 cell. The activated Th2 cells then release IL-4, IL-5 and IL-13. Describe the function of each of these cytokines in type I reactions:

A

IL-4: key factor that causes B cells to switch from IgM to IgE production, induces Th2 cell differentiation
IL-5: Activates eiosinophils
IL-13: promotes IgE production by B cells, induces Th2-cell differentiation of T cells, causes mucussecretion in epithelial cells, and enhances smooth muscle contraction

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6
Q

What are the steps of a type I reaction? Include processes that occur at the time of initial antigen exposure and the subsequent exposure.

A

IgE Ab is induced by an allergen–>IgE binds to Fc receptors on the surface of mast cells/basophils. When the individual is reexposed to the allergen the second time–>the allergen causes cross linking of bound IgE molecules–>the cross linking activates IgE mediated degranulation in mast cells/basophils with release of various mediators the most important of which is histamine, the mediator responsible for the anaphylactiv symptoms.

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7
Q

Type I reactions involve both primary and secondary mediators. Explain the difference between the two.

A

Primary mediators: preformed molecules stored in granules that are directly released
Secondary mediatiors: generated de novo as a consequence of mast cell/basophil activation

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8
Q

Histamine and proteases/hydrolases are primary mediators. What are their functions?

A

Histamine: vasodilation, increases vascular permeability and plasma leak (edema formation), smooth muscle contraction increases secretions (nasal, respiratory)

Protease/hydrolases: tissue damage, activate complement, cleavage of membrane receptors

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9
Q

Leukotrienes B4, C4, D4, and E4 and cytokines are secondary mediators. What are their functions?

A

Leukotrienes: B4–>recruits white blood cell (WBC). C4/D4/E4–>vasodilation, increases vascular permeability
Cytokines: mediate the inflammatory response of the late phase

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10
Q

What are the two phases of type I hypersensitivity reactions?

A
  1. Immediate phase: rapid degranulation of preformed mediators in mast cells/basophils within minutes of reexposure to antigen that cross-links the cell-bound IgE
  2. Late phase: 2-48 hours after antigen exposure; secondary mediators cause an influx, maturation, and activaton of inflammatory cells and increase teir survival in tissue
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11
Q

What are the symptoms of the immediate phase of type I reactions?

A

Edema, erythema, wheal and flare reaction in the skin, itching (skin, eye, nose), runny nose, wheezing

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12
Q

What are the common clinical manifestations of type I hypersensitivity reactions?

A

Skin: urticaria (hives), eczema
Airways: rhinitis, asthma
Eyes: conjunctivitis

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13
Q

What are the consequences of IgE mediated responses in the GI tract, airways and blood vessels?

A

GI tract: increased fluid secretion, increased peristalsis–>expulsion of GI tract contents (diarrhea, vomiting)
Airways: decreased diameter, increased mucus secretion–>expulsion of contents (phlegm, coughing)
BLOOD VESSELS: increased blood flow, increased permeability–>edema, inflammation, and increased lymph flow takes Ag to lymph nodes

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14
Q

What is the most severe form of type I hypersensitivity reactions?

A

Systemic anaphylaxis, which manifests as life-threatening bronchoconstriction and system vasodilation (eg, hypotensive shock)

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15
Q

What are some common causes of anaphylaxis?

A

Peanut, bee venom, drug, and latex allergy

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16
Q

What drugs are commonly given to prevent anaphylactic reactions?

A

Antihistamines, corticosteroids, and cromolyn sodium. Epinephrine can be given as treatment for anaphylactic reactions

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17
Q

How does cromolyn sodium work on mast cells?

A

It stabilizes mast cell membranes preventing degranulation

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18
Q

What do patients with atopic disorders (asthma, eczema and urticaria) have elevated levels of?

A

IgE, Th2 cytokines

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19
Q

Drugs commonly cause hypersensitivity reactions by acting as haptens. What is a hapten and how does this induce hypersensitivity reactions?

A

A hapten is a molecule, which by itself, cannot induce an immune response. The hapten, usually a drug or its metabolite binds to an endogenous protein that then induces antibody formation. The antibody reacts to the hapten (drug or its metabolite) upon subsequent exposure

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20
Q

What are type II hypersensitivity reactions also known as?

A

Cytotoxic hypersensitivity

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21
Q

What reaction occurs in type II hypersensitivity?

A

Antibodies against endogenous cell membrane antigens fix complement causing complement mediated lysis via membrane attack complex

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22
Q 
For each disease associated with type II hypersensitivity, name the target: 
Warm/cold autoimmune hemolytic anemia:
Erythroblastosis fetalis:
Pernicious anemia
Antineutrophil cytoplasmic antibodies (ANCA) vasculitis
C-ANCA
P-ANCA
Goodpasture syndrome
A

Warm/cold autoimmune hemolytic anemia: Self RBC membrane proteins (warm=IgG; cold=IgM)
Erythroblastosis fetalis: Fetal D-Rh antigen
Pernicious anemia: Intrinsic factor (binds B12)
(ANCA) vasculitis: Neutrophil granule protein
C-ANCA: PR3
P-ANCA: Myeloperoxidase
Goodpasture syndrome: Alveolar and glomerular basement membrane

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23
Q 
Rheumatic fever:
Graves Disease:
Myasthenia Gravis:
Lambert-Eaton myasthenic syndrome:
Pemphigus vulgaris:
Bullous pepmigoid:
A

Rheumatic fever: Myocardial ags that cross react with streptococcal ags (possibly the streptococcus M protein)
Graves Disease: Thyroid stimulating hormone (TSH) receptor
Myasthenia Gravis: Acetylcholine receptor
Lambert-Eaton myasthenic syndrome: Presynaptic Ca2+ channels
Pemphigus vulgaris: Epidermal desmosomes
Bullous pepmigoid: Epidermal-dermal hemi-desmosomes

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24
Q

What drugs are associated with warm autoimmune hemolytic anemia? Of these, which drugs are associated with haptens? Which drugs generate autoantibodies?

A

Penicillin and quindine are hapten forming. alpha methyl dopa generates auto antibodies

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25
Q

What test is positive in warm autoantibody disease?

A

Direct antiglobulin (Coombs test)

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26
Q

Cold autoimmune hemolytic disease has an acute and chronic form. What infections are associated with the acute form? What type of neoplasm is associated with the chronic form?

A

Acute form is associated with mycoplasma pneumoniae and infectious mononucleosis (eg, Epstein-Barr virus [EBV]). Chronic form is associated with lymphoid neoplasms

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27
Q

How is the autoantibody in Grave disease different from other autoantibodies?

A

The autoantibody in Grave disease, a thyroid stimulating immunoglobulin (TSI) actually binds and activates the TSH receptor

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28
Q

What type II disease is mediated by an autoantibody that shares the same target as exfoliatin (Staphylococcus toxin in scaled skin syndrome)?

A

Pemphigus vulgaris

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29
Q

What region of autoantibodies attaches to the ag in type II reactions? What region binds the complement?

A

IgG or IgM attaches to the ag at their Fab region and attaches complement at their Fc region

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30
Q

Which of the hypersensitivity reactions are antibody mediated?

A

Types I, II and III

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31
Q

What are type III hypersensitivity reactions also known as?

A

Immune complex hypersensitivity

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32
Q

In type III reactions formation of large antigen-antibody immune complexes deposit into tissues and fix complement. How does activation of complement result in tissue damage? How does this differ from type II hypersensitivity?

A

Complement activation recruits neutrophils, which release proteolytic enzymes and cause tissue damage. This differs from type II in which tissue damage is caused by autoantibody-mediated complement activation (not by formation of large immune complexes).

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33
Q

One important factor that determines if antigen-antibody complexes deposit into tissue is the relative amount of antigen versus antibody. Why do antigen-predominant complexes typically form pathogenic deposits?

A

Antigen-ab complexes are cleared when mononuclear phagocytes bind to ab, resulting in endocytosis of the complex. In ag-predominant complexes, fewer abs means less clearance and a propensity to form pathogenic deposits.

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34
Q

What is a pathology term used to describe type III inflammation in vessels?

A

Fibrinoid necrosis (eosinophilic staining accumulation)

35
Q

What are the two typical type III hypersensitivity reactions?

A
  1. Arthus reaction: local deposition of immune complexes

2. Serum sickness: systemic inflammatory response to immune complexes deposits throughout the body

36
Q

Describe how an Arthus reaction is evoked?

A

Antigen is subcutaneously injected into a host with preformed antibodies to this antigen causing local edema and possible ulceration

37
Q

Hypersensitivity pneumonitis (farmer lung) is an Arthus reaction caused by inhalation of what bacteria?

A

Thermophilic actinomycetes

38
Q

What is the typical clincal presentation of serum sickness?

A

Fever, hives, arthralgia, lymphadenopathy, splenomegaly, and eosinophilia appear days to weeks after ag exposure

Mnemonic: Serum sickness HEALS For Weeks: Hives, Eosinophilia, Arhralgia, Lymphadenopathy, splenomegaly, fever

39
Q

What drug is associated with serum sickness?

A

Penicillin–it can cause type I, II and III via hapten formation

40
Q

What are well known diseases that are resulted from type III immune complex deposition?

A

Poststreptococcal glomerulonephritis, rheumatoid arthritis, and systemic lupus erythematosus

41
Q

What are type IV hypersensitivity reactions also known as?

A

Delayed type hypersensitivity (DTH)

42
Q

What are the two types of type IV hypersensitivity?

A
  1. Classic (tuberculin-like) DTH

2. Contact dermatitis

43
Q

In the first step of classic DTH, macrophages present antigens to CD4+ helper cells and induce CD4+ cells to become what specific subtype? What cytokine secreted by macrophages drives this process?

A

Macrophages induce CD4+ T cells to mature into Th1 cells. IL-12 is the cytokine that drives this process

44
Q

These Th1 cells often remain in the circulatory system as memory cells. When the body is exposed to the ag for a subsequent time, what cells do these Th1 cells activate? What cytokine secreted by the Th1 cells drives this process?

A

Th1 cells activate macrophages. IFN-y is the cytokine that drives this process

45
Q

What functions are enhanced when a macrophage is activated?

A

Increased phagocytosis, increased antimicrobial potency, increased antigen presentation, and further induction of inflammation

46
Q

What functions are enhanced when a macrophage is activated?

A

Increased phagocytosis, increased antimicrobial potency, increased ag presentation, and further induction of inflammation

47
Q

What is seen histopathologically in classic DTH?

A

Granuloma: central core of epithelioid cells (type of y-IFN activated macrophages) with a rim of lymphocytes

48
Q

Which pathogens trigger classic DTH?

A

Mycobacteria and fungi

49
Q

A positive tuberculin skin test is a classic DTH. Describe how a positive test presents

A

Minimal change in the first few hours followed by erythema and in duration of 48 to 72 hours

50
Q

How does contact dermatitis differ from classic DTH?

A

In contact dermatitis, previously sensitized Th1 cells enter the dermis and cause cytokine-mediated cell necrosis as opposed to the granulomatous reactions seen in classic DTH

51
Q

What are common contact allergens?

A

Plants (poison ivy/oak), chemicals, soaps, jewelry metal, topical drugs

52
Q

What are common symptoms of contact dermatitis?

A

Erythema, pruritus, and necrosis of skin with formation of large blisters within 24 hours

53
Q

What is the role of MHC class II proteins on donor cells in graft rejection?

A

Recognized by helper T cells of the host–>proliferation, cytokine production, and “help” to activate cytotoxic T cells to kill the donor cells

54
Q

What are the immunological contraindications to organ transplantation?

A

ABO blood group incompatibility, presence of preformed human leukocyte antigen (HLA) antibodies in the recipient’s serum

55
Q

What does a lymphocyte cross match do?

A

Screens for recipient anti-HLA antibodies against donor lymphocytes

56
Q

What are the typical mechanisms by which transplant recipients are presensitized to donor antigens?

A

Pregnancy, previous transplantation, blood transfusion

57
Q

The mixed lymphocyte reaction is used for MHC class II antigen (D loci) matching. How does it work?

A

Recipient lymphocytes are mixed with irradiated donor lymphocytes and assessed from proliferation. The degree of compatibility is inversely proportional to proliferation by the recipient cells

58
Q

What are the four classes of grafts?

A
  1. Allograft (same species)
  2. Isograft or syngeneic graft (MZ twins)
  3. Autograft (same individual)
  4. Xenograft (transplant bw species)
59
Q

What are the three rejection reactions?

A
  1. Hyperacute rejection
  2. Acute rejection
  3. Chronic rejection
60
Q

What is the time frame of hyperacute rejection?

A

Minutes to hours

61
Q

What mediates hyperacute rejection and what is the specific target on the graft?

A

Preformed abs against graft vascular endothelial ags.

62
Q

What is the cellular results of hyperacute rejection?

A

complement activation leading to endothelial damage, neutrophilic inflammation, and thrombosis

63
Q

How can hyperacute rejection be avoided?

A

Matching and cross matching the ABO blood group of donor and recipient

64
Q

What is the time frame of acute rejection? what if the recipient is treated with immunosuppressive therapy?

A

Within days of transplantation in a nonimmunosuppresed recipient. If immunosuppressed, rejection may occur after months to years

65
Q

What mediates acute rejection and what are the targets of this response?

A
  1. T-cell mediated response (CD4+ and CD8+) to donor vasculature and parenchyma
  2. Humoral rejection with antibodies against vasculature
66
Q

How does each T cell participate in acute rejection?

A

CD8+ cytotoxic T lymphocyte (CTL) recognizes and directly kills donor cells. CD4+ Th1 cells mediate a DTH (type IV) response

67
Q

What causes the delay in acute rejection versus hyperactive rejection?

A

Time lag is due to T cell activation/differentiation and antibody production

68
Q

Accelerated acute rejection occurs when a second allograft from the same donor is given to a sensitized recipient. What is the prinicipal mediator of this process?

A

The presence of memory (presensitized T cells)

69
Q

How long does accelerated acute rejection take?

A

5-6 days in the absence of immunosuppresion

70
Q

What is the time frame for chronic rejection?

A

Months to years

71
Q

What is the main pathologic finding of chronic rejection?

A

Artherosclerosis of vascular endothelium and proliferation of intimal smooth muscle cells

72
Q

What cell causes the vascular pathology that develops in chronic rejection?

A

It is unclear, but is a mixture of immune and nonimmune mediated processes

73
Q

What is the hypothesized cause of chronic rejection?

A

Damage of the allograft during transplant, drug toxicity, and incompatibility of minor histocompatibility antigens

74
Q

What causes minor histocompatibility mismatches between the donor and recipient?

A

Polymorphic self antigens: self proteins that differ in amino acid sequence between individuals

75
Q

What are the drugs used for postoperative immunosuppresion?

A

Calcineurin inhibitors: cyclosporine and tacrolimus
Cell cycle inhibitors: azathioprine and mycophenolate mofetil
Glucocorticoids: prednisone
Antilymphocyte antibbodies: OKT3, Thymoglobulin mTOR inhibitors: rapamycin

76
Q

What is the mechanism behind the use of OKT3?

A

Antibody directed against CD3 which is found on all T cells, leading to decreased T cell numbers

77
Q

How are cyclosporine and tacrolimus immunosuppressive?

A

Cyclosporine prevents the activation of T cells by inhibiting the calcineurin phosphatase which blocks the synthesis of IL-2 and IL-2 receptor

78
Q

How is azathioprine immunosuppressive?

A

Azathioprine is an inhibitor of purine synthesis, thus blocking DNA replication and the proliferation of T cells

79
Q

What are some of the problems associated with immunosuppressive therapy?

A

Drug toxicities, kidney damage, increased viral infections (e.g, cytomegalovirus (CMV), herpes simplex virus (HSV), increased viral associated malignancies (eg, EBV), and other opportunisitic infections

80
Q

What complication is of particular concern in bone marrow transplants?

A

Graft vs. host disease (GVHD) reaction: T cells in the transplanted marrow react against alloantigens of the immunocompromised host

81
Q

What are the three requirements for GVHD to occur?

A
  1. The graft must contain immunocompetent T cells
  2. The host must be immunocompromised so that the graft T cells are not destroyed
  3. The recipient must express antigens foreign to the donor
82
Q

How can GVHD occur even when the donor and recipient have identical classes I and II MHC proteins?

A

Differences in minor histocompatibility antigens

83
Q

What treatments reduce the likelihood of GVHD?

A

Treating the donor tissue with antithymocyte globulin or monoclonal antibodies before grafting and using cyclosporine

Immunology COM (11 decks)

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