Humoral immunity
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Humoral immunity is the aspect of immunity that is mediated by secreted antibodies, produced in the cells of the B lymphocyte lineage (B cell). Secreted antibodies bind to antigens on the surfaces of invading microbes, which flags them for destruction.
Humoral immunity refers to antibody production, and all the accessory processes that accompany it: Th2 activation and cytokine production, germinal center formation and isotype switching, affinity maturation and memory cell generation. It also refers to the effector functions of antibody, which include pathogen and toxin neutralization, classical complement activation, and opsonin promotion of phagocytosis and pathogen elimination.
B cells need two signals to initiate activation. Most antigens are T-dependent, meaning T cell help is required for maximal antibody production. With a T-dependent antigen, the first signal comes from antigen cross linking BCR and the second from the Th2 cell. T dependent antigens contain protein so that peptides can be presented on B cell Class II MHC to Th2 cells, which then provide co-stimulation to trigger B cell proliferation and differentiation into plasma cells. Isotype switching to IgG, IgA, and IgE and memory cell generation occur in response to T-dependent antigens.
Some antigens are T-independent, meaning they can deliver both the antigen and the second signal to the B cell. Mice without a thymus (nude or athymic mice) can respond to T-independent antigens. Many bacteria have repeating carbohydrate epitopes that stimulate B cells to respond with IgM synthesis in the absence of T cell help.
T-dependent responses require that B cells and their Th2 cells respond to epitopes on the same antigen. T and B cell epitopes are not necessarily identical. (Once virus-infected cells have been killed and unassembled virus proteins released, B cells specific for internal proteins can also be activated to make opsonizing antibodies to those proteins.) Attaching a carbohydrate to a protein can convert the carbohydrate into a T-dependent antigen; the carbohydrate-specific B cell internalizes the complex and presents peptides to Th2 cells, which in turn activate the B cell to make antibodies specific for the carbohydrate.
Graft rejection ususally triggers CMIR; Incompatitable blood transfusion triggers HIR. Template:Med-stub
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