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[Fc receptors and immunomodulating effects of immunoglobulins. In vitro study]
Immunomodulating effect of immunoglobulins (Ig) preparations can be investigated by the mean of in vitro models of human B lymphocyte polyclonal activation. Such models concern the final differentiation of mature B lymphocytes into plasma cells. Several stages can be identified, each of them being controlled by distinct regulatory mechanisms: cell proliferation as estimated by tritiated thymidine incorporation, maturation into Ig containing cells, then into Ig secreting cells, and quantification of secreted Ig. In addition to the quantitative control of each stage (potentiation or suppression) a qualitative regulation of the production of each Ig class (IgM, IgG, IgA) can be studied. Depending on experimental protocols, several regulatory mechanisms have been described: 1) polyclonal activation induced by Fc fragments or aggregated Ig acting on monocytes, 2) suppression by aggregated IgG which induce prostaglandin PGE2 release from monocytes, 3) suppression by aggregated IgG interacting with T cell Fc receptors. The latter mechanism selectively decreases the number of IgG containing cells and that of IgG secreting cells, does not change IgG nor IgM containing cell numbers. A comparable suppressive effect can be achieved by Fc receptors purified by affinity chromatography on IgG sorbents. The possible relevance of these various regulatory mechanisms to the in vivo effect of Ig treatment deserves further investigations.
Immunomodulating effect of immunoglobulins (Ig) preparations can be investigated by the mean of in vitro models of human B lymphocyte polyclonal activation. Such models concern the final differentiation of mature B lymphocytes into plasma cells. Several stages can be identified, each of them being controlled by distinct regulatory mechanisms: cell proliferation as estimated by tritiated thymidine incorporation, maturation into Ig containing cells, then into Ig secreting cells, and quantification of secreted Ig. In addition to the quantitative control of each stage (potentiation or suppression) a qualitative regulation of the production of each Ig class (IgM, IgG, IgA) can be studied. Depending on experimental protocols, several regulatory mechanisms have been described: 1) polyclonal activation induced by Fc fragments or aggregated Ig acting on monocytes, 2) suppression by aggregated IgG which induce prostaglandin PGE2 release from monocytes, 3) suppression by aggregated IgG interacting with T cell Fc receptors. The latter mechanism selectively decreases the number of IgG containing cells and that of IgG secreting cells, does not change IgG nor IgM containing cell numbers. A comparable suppressive effect can be achieved by Fc receptors purified by affinity chromatography on IgG sorbents. The possible relevance of these various regulatory mechanisms to the in vivo effect of Ig treatment deserves further investigations.