Cellmediated immunity

Cytotoxic T cells

Upon recognizing antigen-MHC complexes on a target cell, cytotoxic T cells are capable of destroying these cells. Cytotoxicity occurs either by secretion of pore-forming proteins, which help to lyse the cell and allow the entry of granzyme, a proteinase which activates the apoptotic pathway in the target cell, or by the expression of the surface protein Fas which engages Fas ligand on the surface of the target cell, leading to apoptosis of the target.

Activation of macrophages

T cells secreting the cytokines interferon-g, IL-2, and tumor necrosis factor-b can activate cellular effectors, particularly macrophages, rather than antibody production. The subset of CD4 cells with this cytokine profile have been designated Th1 cells, in contrast with the Th2 subset characterized by secretion of IL-4. For example Mycobacterium tuberculosis survives in macrophage endosomes until Th1 cells activate them, enabling the macrophages to fuse their lysosomes with the endosomes in question. Activated macrophages can release their granule contents in 'frustrated phagocytosis' if they cannot engulf the opsonized material.

Eosinophils and mast cells

Eosinophils develop under the influence of IL-5 and act against parasites at inflammatory sites, in contrast with neutrophil activity against bacteria. They are activated by antibody-binding surface Fc receptors, some cytokines, and possibly intrinsic receptors for non-self. Like neutrophils and macrophages, they undergo a respiratory burst to produce reactive oxygen free radicals which kill effectively. They also release proteins damaging to helminths.

Mast cells contain large amounts of the vasoactive amines, such as histamine, which cause vasodilatation and increase vascular permeability, leading to urticaria. They also release other mediators of inflammation, particularly those derived from arachidonic acid. They bind IgE very tightly to their surface, and cross-linking of this leads to mast cell degranulation. Mast cells are potent cellular mediators of inflammation, whose physiological role is probably in defense against parasite infection.

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