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Microbiology 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

four types of hypersensitivity

A

type I: allergy and atopy
type II: antibody-mediated
type III: immune complex-mediated
type IV: delayed-type

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2
Q

type I hypersensitivity is mediated by

A

mast cells

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3
Q

sensitization phase

A

IgE antibody production and binding to Fc receptors on mast cells

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4
Q

activation phase

A

on second exposure to antigen, antigen cross-links membrane bound IgE molecules

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5
Q

effector phase

A

activated cells degranulate releasing pre-formed mediators and release newly synthesized lipid mediators
localized allergic symptoms

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6
Q

late phase

A

~48 hours later
cytokines and chemokines newly produced by mast cells recruit and activate other leukocytes

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7
Q

histamine

A

generated by decarboxylation of the amino acid histidine

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8
Q

most histamine is stored in

A

mast cells

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9
Q

histamine binds to

A

histamine receptors

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10
Q

the action of histamine on a cell depends on

A

the receptor and the cell type

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11
Q

exposure in gastrointestinal tract

A

increased fluid secretion and peristalsis - vomiting and diarrhea

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12
Q

exposure in airways

A

decreased diameter and increased mucus secretion - congestion and airway blockage

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13
Q

exposure to blood vessels

A

increased blood flow and permeability -swelling, more protein in tissues (can increase effector response)

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14
Q

reducing symptoms of Type I hypersensitivity

A

avoiding exposure
asthma meds
anti-histamines block histamine receptors on target cells
corticosteroids
epinephrine
desensitization

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15
Q

how does desensitization/hyposensitization therapy work

A

decreases IgE production by shifting antibody class to IgG and IgA

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16
Q

type II hypersensitivity

A

antibodies bind antigens on surface of cells
usually foreign cells (donated blood, transplanted organ (HLA))
activates NK cells by Fc receptor binding
activation of complement
can be autoimmune

17
Q

type III hypersensitivity

A

immune complexes
large amounts of small, soluble antigen create very small and soluble immune complex
evade clearance and can deposit in tissues
activate complement and lead to recruitment of neutrophils
excessive degranulation damages tissues - free radical generation

18
Q

passive immunity

A

provides strong, immediate, short-lived protection
-maternal antibodies
-convalescent serum
- therapeutic monoclonal antibodies

19
Q

active immunity

A

develops slowly, sometimes requires multiple exposures
-natural infection
-vaccination

long lasting and has memory

20
Q

maternal antibodies

A

trans-placental IgG during gestation
IgA in breast milk coats mucosal surfaces
window of susceptibility

21
Q

anti-toxins immunoglobulin

A

anti-serum contains antibodies that bind to and inhibit bacterial exotoxins
rapid acting and life-saving for diphtheria and tetanus toxin - protection is temporary
originally generated in horses

22
Q

type II reactions cause pathology in what autoimmune diseases

A

systemic lupus erythematosus - antibodies binding DNA or RNA from leukocytes
rheumatoid arthritis - immune complexes in the joints

23
Q

immune complexes in skin lead to

A

arthus reaction

24
Q

what causes farmer’s lung

A

complexes in lungs from Actinomycetes spores in hay
allergic alveolitis

25
Q

molecular mimicry

A

can stimulate Type III reactions against host tissues - post group A streptococcal disease after S. pyrogenes infection

26
Q

serum sickness

A

immune complexes form in blood from foreign proteins
immune complexes accumulate in blood vessel walls, joints and kidneys
this is why antibody therapies are humanized

27
Q

type IV delay type hypersensitivity

A

takes a while for response to initiate
requires T cells activation and recruitment of other cells
cell mediated - no antibodies required
usually Th1 response but can be Th17 as well or be driven by CD8+ T cells
can cause extensive tissue damage if prolonged

28
Q

type IV hypersensitivity - sensitization

A

APC endocytosis/phagocytosis antigen and presents on HLA II to helper T cells
in response to intracellular bacteria
helper cells differentiate and clonally expand to generate effector and memory subsets
Th1 cells responsible

29
Q

type IV hypersensitivity - effector phase

A

Th1 memory cells in tissues encounter APC displaying same activating epitope
activated memory TH cells release cytokines that attract and activate macrophages and other inflammatory response cells, which clear the infected, epitope-bearing cells
24=72h needed for macrophages and T cells to migrate to and proliferate at the antigen site
responses not visible until 24-72h after encounter

Microbiology 2 (18 decks)

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