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Flashcards in Hypersensitivity Deck (21):
1

Type 1 hypersensitivity

allergies/atopic disorders, anaphylatic reactions depend on route of entry and location of responding cells, antigens activate TH2 which release IL-4 to stimulate IgE response which activates mast cells

2 phases: immediate (minutes) phase and late phase (hours) which involves cellular infiltration

2

crosslinking of IgE

activate mast cells to release mediators (granles) such as histamine

3

wheal and flare

part of the immediate response, swelling from leakage-histamine effect and engorged with RBCs

leads to late phase with more widespread swelling and inflammation

4

serotonin

affects vascular permeability

5

SRS-A

slow releasing substance of anaphylaxis, mixture of leukotrienes produced during response

6

TNF

stimulates expression of adhesion molecules on endothelial cells

7

basophils and eosinophils

only expresses IgE receptors after they become activated allowing them to bind IgE. Once activated, they degranulate and increase in number.

8

response to subcutaneous allergen

ex. insect allergen, results in localized swelling, urticaria (hives), angiodema (deeper, diffuse swelling), eczema

used to test skin for allergies (RAST assay)

9

responses to inhaled allergen

allergic rhinitis, results in the sensitization of mast cell and eosinophils producing mucus.

peptides derived from pollen grains are presented by APCs to activate antigen specific T cells which secrete IL-4 resulting in isotype switch to IgE.

10

allergic asthma

can result in both an acute response and chronic response

for the acute response, mast cell capture antigen and inflammatory mediators contract smooth muscle, increase mucus secretion, and increase blood vessel permeability

11

chronic asthma

can occur in the absence of allergen - persons with chronic asthma are hyper responsive to other irritants in the air such as cigarette smoke

cellular infiltrate and inflammation can lead to tissue remodeling.

12

reaction to absorbed allergen

food allergies, ingestion of antigen activates mucosal mast cells, antigen diffuses into blood vells and can cause urticaria, vomiting, diarrhea. mechanism is similar to what body does to expel parasites.

13

systemic allergen - systemic anaphylaxis

most severe form of Type 1 - antigens include drugs, serum, venom, peanuts

antigen in bloodstream enters tissues and activates connective mast cells throughout body

14

hygiene hypothesis

poorer hygiene results in exposure to TH1 inducing infections which protect against allergy

15

Counter Regulation Hypothesis

infections lead to production of IL-10 and TGF-beta which downregulate both TH1 and TH2 responses so less hypersensitivity

16

treatment to Type 1 hypersensitivity

avoid allergen, treat symptoms, desensitization, allergenic peptide vaccination, anti-IgE, anti-cytokines

17

Type 2 hypersensitivity

mediated by IgG, drug induced or blood transfusion, antibodies bind to cell associated antigen or cell surface receptor and fix complement, can lead to lysis of RBCs or platelets

18

Type 3 hypersensitivity

formation of large latticed immune complexes leading to downstream cellular damage depending on what tissue site they deposit

can lead to arthus (localized) reaction or serum sickness

19

serum sickness

formation of antigen:antibody complexes, occurs after development of antibody to antigen (7-10 days), may occur after large amounts of foreign protein in antisera, generally resolves itself

20

Type 4 hypersensitivity

mediated by TH1 cells, reactions include delayed type hypersensitivity (TB test), contact hypersensitivity (poison ivy), celiac disease (gluten sensitive enteropathy)

21

treatment for types 2, 3, 4 hypersensitivity

avoidance, anti-inflammatories, reduction of immune response (steroids), regulatory T cells (peptide vaccination), blocking of effector mechanisms