Alteration in Immune Response
Alteration in Immune Response
immune response
Mechanism
IgE-mediated—mast cell degranulation
Trigger
binding of an allergen to a specific IgE that is found on the
surface of mast cells or basophils
Subsequent exposure
The sensitizing allergen binds to the cell associated IgE and triggers a
series of events that ultimately lead to degranulation of the sensitized
mast cells or basophils, causing release of their allergy-producing
mediators.
Type I mediators
The primary (preformed) mediators of allergic reactions include:
Histamine
potent vasodilator that increases the permeability of capillaries and
venules
bronchoconstriction
increased secretion of mucus
Acetylcholine
bronchial smooth muscle contraction
dilation of small blood vessels
Adenosine
Chemotactic mediators - cytokines that recruit and activate a
variety of inflammatory cells.
Neutral proteases
generate kinins and cleave complement components to produce
additional chemotactic and inflammatory mediators
Type I mediators
Secondary mediators - generated from arachidonic acid in the mast
cell membrane:
Leukotrienes
Prostaglandins
Platelet aggregation
Histamine release
Bronchospasm
More rarely, they may result from ingested allergens (seafood, nuts,
legumes).
They tend to have high serum levels of IgE and increased numbers
of basophils and mast cells.
Localized Atopic Disorders
Although the IgE-triggered response is likely to be a key factor in the
pathophysiology of the disorders, it is not the only factor.
Mechanism
Formation of antibodies (IgG, IgM) against cell surface antigens.
Complement usually is involved.
E. g.
Autoimmune hemolytic anemia
Type II (cytotoxic)
hypersensitivity
reactions are the end
result of direct
interaction between IgG
and IgM class antibodies
and tissue or cell surface
antigens, with
subsequent activation of
complement- or
antibody-dependent cell-
mediated cytotoxicity.
Type III, Immune-Complex Disorders
Mechanism
Formation of antibodies (IgG, IgM, IgA) that interact with
exogenous or endogenous antigens to form antigen - antibody
complexes.
Trigger:
exogenous antigens such as viral and bacterial proteins
Mechanism:
The donor T cells recognize and attack the antigens - the host
HLA.
The greater the difference in tissue antigens between the donor
and recipient, the greater is the likelihood of GVHD.