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IHL Exam 2 > Hypersensitivities > Flashcards

Hypersensitivities Flashcards

1
Q

Hypersensitivity

A

injurious or pathologic immune responses

occurs in two situations:
disregulation/uncontrolled
immune response directed against self

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2
Q

Immediate hypersensitivity

A

Type I

IgE and mast cell mediate reaction to certain antigens that causes rapid vascular leakage and mucosal secretions, often followed by inflammation

ALLERGIES (atopic), asthma

involves TH2 cells

has both immediate hypersensitivity phase and latent-phase reaction

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3
Q

Steps in immediate hypersensitivity

A

activation of Th2 cells by binding to B cell that has been exposed (first time) to allergen

antigen activation of TH2 cells and stimulation of IgE class switching in B cells (b/c of IL-4 and IL-13 produced by TH2 cells)

binding of the IgE to Fc receptors on mast cell
note IgE also activates eosinophils

Subsequent exposure to allergen/antigen

release of mast cell mediators

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4
Q

IgE

A

1/2 life in serum is 2 days

1/2 life bound to FcR on Mast cells and basophls is 10 days

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5
Q

late-phase reaction

A

inflammatory component of immediate hypersensitivity that occurs several hours after subsequent antigen/allergen exposure

responsible for the tissue injury that results from repeated bouts of immediate hypersensitivity

mediate by mast cell mediator and cytokines that recruit neutrophils and eosinophils to the site of the reaction

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6
Q

what does IgE promote

A

promotes TH2

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7
Q

how is immediate hypersensitivity a T-cell dependent adaptive immune response ?

A

reliant on Th2 cells to produce IL-4 and IL-13 that switch to IgE

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8
Q

Classical antigens

A

Constant challenge b/c you can’t remove allergy to a antigen

inhaled in very low doses

eaten in large doses

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9
Q

immunological priming

A

primed the system to make more memory cells

making more plasma cells with IgE

so making more IgE higher affinity binds to antigen…. loading of mast cell

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10
Q

what is needed in order to activate mast cell?

A

must cross-link IgE’s in order to get activation of cell

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11
Q

Clinical syndromes causes by Type I hypersensitivities

A

Allergic rhinitis

food allergies

bronchial asthma

Anaphylaxis

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12
Q

late phase reaction

A

part of type I immediate hypersensitivity

occurs 4-6 hours after initial type I reaction

persists 1-2 days

infiltration of PMN’s, eosinophils, macrophages, lymphocytes

due to mast cells releasing TNF alpha and IL-1 which leads to increased expression of adhesion molecules on endothelial cells

mast cells release IL-8, IL-3, IL-5, GM-CSF–> hematopoietic

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13
Q

antibody mediated (type II) hypersensitivity

A

initiating antigen is a surface

IgG, IgM, FcR, C’ SURFACE antigen

can happen by anti-tissue antibody:

  • antibody/antigen complex activates C’ (classical)
  • antibody/antigen complex interacts with FcR’s on effector cells (ie. neutrophil)
  • alternative C’ pathway C3b on surface
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14
Q

effects of antibody mediated hypersensitivity

A

local inflammation and tissue injury

antibodies bound to Fc receptors on effector cells induce effector cells to release ROS and lysosomal enzymes that damage the tissues

complement cascade can “poke holes” by the MAC and also the away parts can induce inflammation by recruitment

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15
Q

hemolytic disease of the newborn

A

mother makes IgM b/c she sees the baby rh antigen during first pregnancy

class switches to IgG

during second pregnancy the mothers memory cells recognize another rh antigen in baby

mothers IgG attacks babies RBC’s

can treat with Rhogam which prevents B cell activaiton and memory cell formation in the first place

RhD antigen in babies is most common

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16
Q

Transfusion reactions

A

?? slide 25 hypersensitivities

17
Q

Autoimmune Hemolytic anemias

A

see garrisons CSI

18
Q

Myasthenia gravis

A

extreme muscle weakness

make self antibodies to acetylcholine receptors

antibody inhibits acetylcholine receptor so acetylcholine cannot activate

19
Q

Type III hypersensitivites

Immune complex

A

IgG/IgM/FcR/C’ SOLUBLE antigen

immune complexes of Ab/Ag/C’ in circulation

complexes deposit in tissue–> leads to pathology

three groups of pathology:

  • persistent infections
  • autoimmune diseases
  • inhalation of antigen
20
Q

CR1

A

on RBC’s

binds immune complexes and brings them to the liver and spleen for removal

21
Q

when we have more IC’s that can be cleared….

A

start to bring in basophils and platelets and IC’s act on them, which produce vasoactive amines (histamine)

this causes endothelial cell to get leaky, pull apart, and creates an area where the IC can settle into

increase in vascular permeability

22
Q

what happens after the IC deposits into the blood vessel wall?

A

induces platelet aggregation and C’ activation

microthrombi form on the exposed collagen of the basement membrane of the endothelium

neutrophils are attracted to the site by the C’ products and lead to further damage of the area

Increases in blood pressure and vascular turbulence increases complex deposition

thrombocytopenia

23
Q

desensitization

A

allergy shots

given small amounts of antigen and trying to build IgG to block bind antigen before it binds IgE

can cause arthus reaction in which there is a formation of marked edema and hemorrhage 4-10 hours after allergy shot due to Ag/Ab precipitation

can lead to necrosis
farmer’s lung

24
Q

serum sickness

A

induced by systemic administration of a protein antigen, which elicits an antibody response and leads to formation of circulating IC’s

the individual makes antibody responses against the injected foreign antibodies

the IC’s deposit in blood vessel walls and tissues

leads to arthritis and glomerulonephritis, systemic vasculitis

25
Q

type IV hypersensitivities

A

delayed type hypersensitivities

antigen specific T cells are the effector cells

result from inflammation caused by cytokine produced by CD4 T cells (Th1 mostly) and/or killing of host cells by CD8+ CTL’s

26
Q

DTH

A

DTH reactions are manifested by infiltrates of T cells and blood monocytes in the tissues, edema and fibrin deposition caused by increased vascular permeability in response to cytokines produced by CD4 + T cells, and tissue damage induced by leukocyte products, mainly macrophages, activated by the T cells

27
Q

representative immunopathologic disease for DTH (type IV)

A

contact dermatitis

granuloma formation

28
Q

Three types of DTH

A

Contact
Tuberculin
Granulomatous

29
Q

Contact DTH

A

48-72 hours reaction

clinical appearance is eczema

antigen is epidermal, reaction occurs at point of contact with allergen

two stages:
sensitization (10-14 days)
elicitation

30
Q

Granulomatous DTH

A

21-28 days later

31
Q

Sensitization stage of contact DTH

A

takes 10-14 days

hapten forms (poison oak antigen + protein)
hapten taken up by langerhan cells
goes to lymph nodes and presents to CD4+ T cells
building effector memory cells

32
Q

Elicitation stage of contact DTH

A

CD4 T cells recruited to site of contact

CD4 (Th1 mostly) secrete IFN-gamma and other proinflammatory cytokines that activate macrophages

33
Q

Tuberculin

A

type of DTH

induced by soluble antigen

used to test for tuberculin skin test–> looking for recall response to previously encountered Ag

also can meaure someones cell-mediate immunity and see if someone has a response

34
Q

Granulomatous DTH

A

usually results from persistence of bacteria or virus within macrophage of intracellular microorganisms able to resist macrophage killing or other particles the cells is unable to destroy

occurs with chronic infections associated with TH1 like responses

can also occur in the absence of infection (foreign body or non-immune)

35
Q

Granulomatous reaction

A

persistance of antigen leads to differentiation of macrophage to epitheloid cells and the fusion to form giant cells.

granuloma formation is driven by T cell activation of macrophage and is dependent on TNF

36
Q

chronic diseases manifest type IV granulomatous hypersensitivities

A

tuberculosis

leprosy

crohn’s

IHL Exam 2 (14 decks)

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