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Immunology-Nicole > Hypersensitivity Lecture Objectives > Flashcards

Hypersensitivity Lecture Objectives Flashcards

1
Q

List the Gell and Coomb’s Classification of hypersensitivity

A

Type I: Immediate hypersensitivity
Type II: antibody mediated hypersensitivity
Type III: Immune Complex mediated hypersensitivity
Type IV: Cell mediated hypersensitivity

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2
Q

What is the sensitization phase for hypersensitivity type I

A

Occurs when antigen exposure induces B cell activation leading to IgE production with IgE binding to FceR on mast cells and basophils. IgE antibodies bind to high affinity Fc epsilon receptors present on mast cells and basophils awaiting re exposure to the initiating antigen.

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3
Q

What is the effector phase for hypersensitivity type I?

A

Early phase -> triggered by products of mast cell degranulation (result of histamine release)

Late phase – > sustained inflammation and involves Th2 cells, eosinophils and basophils.

Th2 secretes IL-5 which leads to mobilization of eosinophils

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4
Q

Describe the clinical manifestations of hypersensitivity reaction rhinitis

A

refers to inflammation of the nasal mucous membranes, sneezing, nasal congestion and watery discharge from the eyes following antigen exposure.

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5
Q

Describe the clinical manifestations of hypersensitivity reaction asthma?

A

inflammatory processes stimulate repair mechanisms that lead to structural changes in the bronchial tree (airway remodeling).

The bronchial wall thicken, and the airway narrows.

wheezing occurs if there is bronchoconstriciton

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6
Q

Describe the clinical manifestations of anaphylaxis

A

systemic, potentially fatal, reaction that affects both the cardiovascular and respiratory systems, leading to cardiac arrhythmia and hypotension

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7
Q

Prophylactic pharmacological interventions include anti-histamines or sodium cromoglycate. What is the rationale for prophylactic intervention for these drugs

A

Anti-histamines are H1 histamine receptor antagonists that competitively inhibit binding to H1-binding sites. (no effect on bronchoconstriction)

Sodium Cromoglycate stabilizes the mast cell and basophil membranes, decreasing the release of inflammatory mediators following crosslinking of cell bound IgE by antigen.

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8
Q

Epinephrine and steroids are NOT prophylactic. Explain the rationale for administering each

A

Epinephrine –> important antidote following exposure to agents triggering severe, life threatening immediate type hypersensitivity reactions. Provides transient protection

Steroids–> control the persistent/recurrent symptoms over the four to eight hours post exposure. block late phase reactions after early phase anaphylaxis

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9
Q

What is the mechanism underlying desensitization (allergy shots)

A

immunization with antigen that stimulates the production of IgG antibodies instead of IgE, following promotion of naive CD4+ T cells to differentiate to Th1 phenotype.

IgG antibodies should neutralize the antigen before it reacts with the cell bound IgE.

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10
Q

What is the limitation of the skin test ?

A

used to determine sensitivity to different allergens but the problem with that could be anaphylaxis during the test so an in vitro antigen specific radioallergosorbent (RAST) test is used.

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11
Q

what is the limitation of the RAST test?

A

RAST measures quantitatively the allergen specific IgE antibodies present in the serum. The limitation of this test is that IgE bound to mast cells are not estimated, potentially leading to false negative results. Also IgG antibodies specific for the antigen may competitively bind the antigen, preventing detection of IgE.

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12
Q

People with allergies to nuts and shellfish, or insect stings should carry three things. List these and when each should be used

A
  1. An epi-pen (to deliver immediate epinephrine in the event of exposure)
  2. Benadryl (to be taken after #1,en route to the hospital)
  3. A medic-alert bracelet (in case they can not communicate their significant medial history)
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13
Q

Type II (antibody mediated) sensitization phase

A

marked by production of IgG and IgM antibodies specific for a cell surface antigen

antigen either constitutive of the cell or exogenous antigens that have bound to the cell surface

any cell may be target

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14
Q

Type II (antibody mediated) effector phase

A

No re-exposure needed –> antigen has not been eliminated upon primary exposure

destruction of cells via ADCC by NK cells (perforin and granzyme)
classical pathway (due to IgM and IgG production)
opsonin mediated phagocytosis due to deposition C3b on target cells
opsonin mediated phagocytosis with IgG and FcgammaR

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15
Q

Type III (immune complex mediated) sensitization phase

A

IgM and IgG antibodies bind with soluble antigens to form immune complexes

in autoimmune diseases: immune complexes formed in excess - over capacity of the reticuloendothelial system (normal immune clearance mechanism)

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16
Q

Type III (immune complex mediated) effector phase

A
  1. C5a –> chemotactic for neutrophils
    immune complexes formed in excess –> deposit capillary wall –> stimulate complement activation –> generates anaphylotoxins (c5a) and C3b opsonin
    C5a bind mast cells/basophils –> increases vascular permeability
  2. Neutrophils activation by FcgammaR
    activated neutrophils secrete inflammatory mediators –> ROIs, proteolytic enzymes, elastase and collegenase
    damaged endothelium exposing subendothelium this activates intrinsic coagulation pathway –> bradykinin and kallikrein are made
    frustrated phagocyte –> can no phagocytized
17
Q

Is a transfusion reaction type II or III and why?

A

type II

IgM antibodies, isohaemagglutinins, bind to these glycoproteins on red cells, and activate complement leading to lysis or opsonin mediated (C3b) phagocytosis

18
Q

Is hemolytic disease of the newborn (Erythroblastosis fetalis), primarily due to Rh incompatibility type II or III?

A

type II

negativeRh mom with positiveRH progeny –> Mom exposed after any placental transfer, can be prior to current pregnancy –> IgG or C3b phagocytosis

19
Q

Are autoimmune reactions to cellular antigen or tissues and hyperacute rejection of transplanted tissue, type II or III?

A

Type II

20
Q

What autoimmune diseases are associated with type II hypersensitivity?

A
  1. Goodpasteur’s syndrome –> glomerular and pulmonary basement membranes are a site of immune mediated damage due to the formation of antibodies to basement membrane antigens (Common to both kidney and lungs)
  2. Chronic Idiopathic uticaria –> form antigen to Fc part of IgE antibody or Fcepislon portion on mast cell –> only cutanous mast cell – >itchy and annoying
21
Q

what autoimmune diseases are associated with type III hypersensitivity?

A
  1. Systemic Lupus Erythematosus (SLE) –> kidney glomeruli causes glomerulonephritis
  2. RA –> complexes deposited on joints
  3. Farmer’s Lung –> complexes deposited in lungs
  4. Arthus Reaction –> localized after subQ or intradermal injection of same antigen (prior to exposure to antigen)
  5. Serum Sickness –> Tetanus vaccine given less than 5 years apart
22
Q

Type IV hypersensitivity reaction sensitization phase ?

A

naïve CD4+ T cells (Thp), are activated and differentiate to Th1/Th2 cells secreting cytokines

Th cells clonally expand, with some becoming memory cells, providing immunosurveillance as they circulate via blood and lymph

23
Q

Type IV hypersensitivity reaction effector phase ?

A

Re-exposure to antigen –> activate Th1 memory cells –> Antigen re-introduced topically or intradermally

Persistent intracellular existence of microbe –> tissue damage via inflammatory mediators and cytokines secreted by activate neutrophils and tissues MO after phagocytosis

24
Q

What is an example of a chronic type IV hypersensitive reaction

A

Granulomatous inflammation: granuloma formation

CD4+

25
Q

what is an example of an acute type IV hypersensitive reaction?

A

Mantoux reaction through PPD: induration

CD4+

26
Q

what is an example of a contact type IV hypersensitive reaction?

A

Poison Ivy dermatitis: pruritic/rash

CD8+

27
Q

Describe the Mantoux test

A

PPD skin patch test–> takes 28 hours
look at 46 and 98 hours to see if there is any change

TB skin test –> 48 hours look for inflammation and swelling

28
Q

What is an example of a chronic type IV hypersensitive reaction

A

Granulomatous inflammation: granuloma formation/CD4+
Granuloma formation in TB/sarcoidosis (or chronic HSN pneumonitis)
Granulomatous Inflammation–> persisting antigens that escaped phagocytosis

29
Q

what is an example of an acute type IV hypersensitive reaction?

A

Mantoux reaction through PPD: induration/CD4+

memory Th1 cells secrete IFNgamma and TNF activating MO

30
Q

what is an example of a contact type IV hypersensitive reaction?

A

Poison Ivy dermatitis: pruritic/rash/ CD8+
Urishol from the ivy is a hapten that binds to a carrier protein which stimulates memory Th1 cells to generate immune response
2 days post exposure
Different that urticara –> hives and skin damage –> itchy and not due to IgE

31
Q

describe how the arthus reaction was discovered in rabbits

A

rabbits were given repeated local injections of an antigenic substance, such as horse serum.

The reaction to early injections consists of transient edema, then of hyperemia and edema, and following many injections becomes hemorrhagic and necrotic

Immunology-Nicole (20 decks)

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