Genetics of resistance to bacterial and parasitic infection / edited by D. Wakelin and J.M. Blackwell.

Date:
1988
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Licence: Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

Credit: Genetics of resistance to bacterial and parasitic infection / edited by D. Wakelin and J.M. Blackwell. Source: Wellcome Collection.

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    12 Genetics of Resistance to Bacterial and Parasitic Infection nature of the help provided by Th cells in this process is still disputed but it probably includes physical reorientation of determinants as well as release of soluble factors which trigger В cell activation. A degree of MHC restriction is also required for successful interaction. The net result of the interaction is transformation and proliferation of the В cells, with a proportion of the cells becoming plasma cells. These then release antibody with specificity for the antigenic determinant concerned. Initially plasma cells release IgM, but may later switch, under Th cell control, to the production of IgG, IgA and IgE. A number of antigens can elicit antibody responses without the involvement of T cells. Such T independent antigens are usually carbohydrate molecules, characteristically with a highly repeated unit structure. Repetition of an antigenic determinant along the length of a molecule may be one factor which renders T cell help unnecessary. As far as infectious organisms are concerned the most important T independent antigens are those deriving from bacteria, and in particular from the carbohydrate components of bacterial cell walls, for example the lipopolysaccharide component of the endotoxin found in gram-negative species. T independent antigens elicit IgM-dominated antibody responses. 1.5.1.У Non-lymphoid cells T cells release a number of factors (lymphokines) which influence both the production and the activity of non-lymphoid cells (table 1.2). Mention has already been made of T cell control of macrophages. Activation of macrophages in response to lymphokine production, and control of their localization, plays an important role in combating infection by microparasites and by the larval stages of certain macroparasites (e.g. schistosomes and filarial nematodes). T cells also interact with mast cells, not only through the release of antigen-specific factors capable of binding to their membranes (see above) but (in the case of mucosal mast cells) also through the release of factors which regulate production and differentiation of precursor cells. A similar influence is exerted upon the development of neutrophils and eosinophils-from bone-marrow precursors. Regulation of these cell types is important for the resolution of many types of infections against which mast cells, neutrophils and eosinophils, either separately or in conjunction, can play effector roles. 1.5.2. Antibody-mediated responses The contribution of antibodies to resistance is manifold and no more than a brief outline can be attempted here. Combination of antibody with specific antigenic determinants present on the surfaces of infectious organisms can initiate a variety of events which lead to the inactivation or the death of the organism. Agglutination by antibody-mediated cross-linking of determinants inactivates the organisms, reduces their infectivity and facilitates their phagocytosis. Simple binding of antibody as such can interfere with correct attachment to, or penetration of, host cell surfaces and thus effectively prevent infection from taking place. Facilitation of host cell adherence