Human Anatomy, Physiology, and Medicine. Anything human!
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What is the difference between IgG and IgE which causes allergies to occur and why do some allergies cause severe reactions like anaphlaxis and others just cause a rash. Also are allergies genetic or can be passed from mother to baby by placenta or breast milk or are they just in the one individual?
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Allergies mediated by IgG are known as type II & III (hypersensitivity), which IgG will engage Fc receptor on phagocytes and NK cells, and complement-mediated effector mechanisms to varying degrees, depending on the subclass of IgG and the nature of the antigen involved.
- Type II responses are directed against cell-surface or matrix antigens. Example: some drug allergy, penicillin.
- Type III responses are directed against soluble antigens, and tissue damage involved is caused by responses trigerred by immune complexes. Example: serum sickness, Arthus reaction.
Allergies mediated by IgE is known as type I, which IgE will induce mast-cell activation. This is directed to soluble antigen. Example: allergic rhinitis, asthma, systemic anaphylaxis.
The allergic reaction is various, from rash to systemic anaphylaxis, depends on the type of antigen and the effector mechanism as I mentioned above.
Allergic reactions is mostly individual. However it is stated that allergic asthma is gentics and inherited, but I still have no idea about this.
I'll add a little here..IgE is also drawed out when we got the first allergen and when it comes to the second, IgE will bind the FcE-R in mast cells and causing an influx of Ca2+ and resulting degranulation (histamine secretion). Correct me if I'm wrong..
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Yeah, that's the detail... Want to get more detail, take this:
IgE secreted by plasma cells bind to the high-affinity IgE receptor on mast cells, basophils, and activated eosinophils. When the surface-bound IgE is cross-linked by antigen, these cells express CD40L and secrete IL-4. CD40L will build a cognate interaction with CD40 on the surface of the activated B cell, whereas IL-4 will turn binds to IL-4 receptors (IL-4R) on the same activated B cell. These stimulate isotype switching by B cells and the production of more IgE. These interactions can occur in vivo at the site of allergen-triggered inflammation, for example in BALT (bronchial-associated lymphoid tissue).
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