University:
York University
Course:
SC/BIOL 3120 | Immunobiology
Academic year:

2023
Views:

286

Pages:

2
Author:

Niklas

Type | Hypersensitivity Mediators Histamines formed by decarboxylation of histidine (amino acid) binds to one of four possible histamine receptors Hi binding induces contraction of intestinal/ronchial smoothe muscles, increased permeability of venules, & mucous secretion Ha binding increases vasopermeability & vasodiolation, stimulates exscrine glands, and increases stomach acid; ALSO suppresses degranulation of mast cells/basophils in a negative feedback loop Hs less involved in type 1; modulates neurotransmitter activity in CNS mediates mast cell chemolasis Leukotrienes and Prostaglandins Secondary mediators formed when membrane phospholipids are enzymatically cleaved →active at nanomole levels (1000s more effective than hamine at inducing branchesanstriction more potent stimulators of vascular permeability and mucous secretion considered to be a major cause of asthma symptoms. cytokines and chemokines mast cells and basophils release several of these signaling mulecules -IL-4 and 11-15 stimulate Tut responses to increase IgE panduction IL-5 recruits and activates eosinophils -TNF may contribute to shock in systemic anaphylaxis -GAGL-3 acts as a chemotactic factor, attracting other cens GM-C3F stimulates production and activation of matloid cells some granulocytes. Early vs Late Responses Early Response occuts within minutes of allergen exposure medialed by mast cell granule release of histamine, leukotriene, and prostaglandin Lake Responses occurs hoors after antigen exposure a result of recruited ceils cytokines teleased from mast cells increased expression of chemokines and CAMs on endothelium facilitating influx of neutrophils, casinophils, and Tuz cells - eosinophits play a role in late-phase recruiting neutrophils and degrunulation The Wheal and Flave Alth