Unregistered101
10-06-2006, 01:13 PM
We usually say that an anaphylactic reaction is mediated by release of vasoactive substances from mast cells and basophils in the context of type I hypersensitivity reaction. And we stop there. Well, I just got a question that tests the deeper levels of this.
Basically what happens is in genetically predisposed individuals, exposure to certain compounds (allergens..) leads to antigen recognition by T lymphocytes. A subset of T lymphocytes, TH 2 cells, secrete IL-4 and IL-5, which stimulate B lymphocytes to produce antigen specific IgE. IgE attaches to mast cells by binding Fc-receptors on their surface. Upon reexposure, binding of the antigen to mast cell-IgE triggers a degranulation response with subsequent release of vascoactive mediatos, such as histamine, and arachidonic acid metabolites, causing vasodilation, vascular leakage, and contraction of bronchial smooth muscle.
This is my 2 cents contribution. I hope it helps...
Basically what happens is in genetically predisposed individuals, exposure to certain compounds (allergens..) leads to antigen recognition by T lymphocytes. A subset of T lymphocytes, TH 2 cells, secrete IL-4 and IL-5, which stimulate B lymphocytes to produce antigen specific IgE. IgE attaches to mast cells by binding Fc-receptors on their surface. Upon reexposure, binding of the antigen to mast cell-IgE triggers a degranulation response with subsequent release of vascoactive mediatos, such as histamine, and arachidonic acid metabolites, causing vasodilation, vascular leakage, and contraction of bronchial smooth muscle.
This is my 2 cents contribution. I hope it helps...