Autoimmune
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IgG
Most abundant of ABs Activates complement proteins
IgA
Attached to epithelial cells Prevents microbes from crossing mucus membrane
IgM
Activates complement proteins Makes bacteria cells clump together
IgD
Never exposed to antigens When they are exposed, they will create a mold of the antigen that can be used to make antibodies
IgE
Immediate allergic rxns & parasites
T-cells
Responsible for cell-mediated immunity where they kill targets directly or stimulate activity of other leukocytes
Adaptive immunity can be
Active or passive
Lymphoid organs contain
Large quantities of immune cells
Lymphoid organs
Lymph nodes, spleen, tonsils, appendix, bone marrow, thymus
Primary immune response
Latent period of 7-14 days following exposure before antibodies can be produced. Dominated by IgM with some IgG
Secondary immune response
Occurs upon subsequent exposure to an antigen. Antibodies appear faster because memory cells recognize antigen and can make a faster immune response.
Autoimmunity
Immune reaction to self-antigens
Alloimmunity
Immune reaction to tissues of another individual
In hypersensitivity, what is the body injured by?
The immune response NOT the antigen/allergen
Immediate hypersensitivity rxn
Minutes to hours after exposure
Delayed hypersensitivity rxn
Hours to appear, at severity days after re-exposure to antigen
Anaphylaxis
Most rapid and severe rxn
Type 1 rxn
IgE mediated Hay fever, allergies Immediate rxn
Type 2 rxn
AB mediated Tissue-specific Immediate
Type 3 rxn
Complement-mediated immune disorders Ag-AB complex deposited in tissues Immediate
Type 4 rxn
T-cell mediated rxn Delayed rxn
Type 1 rxn allergen
Contained within particle too large to be phagocytosed or protected by a nonallergenic coat.
Type 1 Pathogenesis
T-helper cells differentiate B cells into specific IgE-producing cells IgE antibodies attach to receptors on mast cells or basophils Allergen binds to cell-associated IgE Binding triggers degranulation of mast cells/basophils to release histamine
Type 1 primary response
-Occurs 5-30 minutes after exposure, subsides within 60 -Mediated by mast cell degranulation