Immune response mast cells

Fig.1. Mast cells bridge innate and adaptive immunity. Activation of mast cells by TLR ligands induces a fast local inflammatory response. Mast cell-derived mediators also promote the migration of antigen-laden LCsfrom the skin to the regional LNs, where a specific adaptive immune response is induced.

Ragweed pollen, bee stings and other antigens elicit immune responses ranging from mild wheezing to potentially-fatal anaphylactic shock in sensitive individuals. Histamine, a chemical produced in many human tissues, mediates many of these responses. Mast cells and basophils release histamine in response to a variety of antigens. 

An allergen is usually an inert substance (e.g. pollen, house dust mite faeces) that in some individuals can trigger the generation of an (inappropriate) antigenic response. Mediated by TH2 lymphocytes, it causes B-Lymphocytes to produce lgE. Subsequent exposure of a sensitized individual to the allergen is therefore able to cross-link IgE antibodies on the surface of mast cells and trigger an immune response and histamine release. 

A cascade of proteins of the immune response that can be triggered by antigen-antibody complexes and by the innate immune system (e.g. exposure to microbial polysaccharides) to raise the immune response. Complement proteins can detect and bind to foreign material or immune complexes and label them for phagocytosis. They can also cause inflammation by directly degranulating mast cells and releasing chemokines to recruit other immune cells into the affected area. 

Type I allergic reactions are inappropriate immune responses to an allergen with preferential synthesis of immunoglobulin E (IgE), a special antibody class, which binds to mast cells and basophilic granulocytes via Fee receptors. Binding of the allergen to the cell-bound IgE initiates the rapid release of allergic mediators, most prominently histamine, and the de novo synthesis of arachidonic acid metabolites and cytokines, which are responsible for the clinical symptoms. 

Syk and ZAP-70 are early intermediates in the transduction of signals from immune receptors, including the B- and T-cell recqrtors for antigen, activatory natural killer-cell receptors, the mast cell and basophil receptor for IgE, and the widely distributed receptors for the Fc portion of IgG. Immune receptors control checkpoints in lymphocyte development and serve to integrate the responses of innate and acquired immunity. 

A large number of cells are involved in the immune response and all are derived fiom the multipotential stem cells of the bone marrow. The predominant cell is the lymphocyte but monocytes-macrophages, endothelial cells, eosinophils and mast cells are also involved with certain immune responses. The two types of immunity (humoral and cell-mediated) are dependent on two distinct populations of lymphocytes, the B cells and the T cells respectively. Both the humoral and the cell-mediated systems interact to achieve an effective immune response. 

Lee, T.D.G. and Wakelin, D. (1982) The use of host strain variation to assess the significance of mucosal mast cells in the spontaneous cure response of mice to the nematode Trichuris muris. International Archives of Allergy and Applied Immunity 67, 302—305. 

Aoki, I., Itoh, S., Yokota, S., Tanaka, S.I., Ishii, N., Okuda, K., Minami, M. and Klinman, D.M. (1999) Contribution of mast cells to the T helper 2 response induced by simultaneous subcutaneous and oral immunization. Immunology 98, 519-524. 

Wang, H.W., Tedla, N., Lloyd, A.R., Wakefield, D. and McNeil, P.H. (1998) Mast cell activation and migration to lymph nodes during induction of an immune response in mice. Journal of Clinical Investigation 102, 1617-1626. 

The regulation of mast-cell activity by biologically active peptides is an area of research, the rapid growth of which has been sparked in part by this intense interest in the interactions between neural, endocrine and immune systems [4, 26, 41] and in part by the recognition that activation of mast-cell secretion as a purely allergic IgE-dependent event is undoubtedly too restrictive. The involvement of the mast cell in the inflammatory response, for example, has for years been suspected to involve a number of non-immunologic, IgE-inde-pendent factors [24,42], Direct evidence for peptide involvement, however, has... 

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