Polyclonal inhibitors

While polyclonal activators possess polyclonal inhibitory potentialities, the polyclonal inhibitors listed in Table 2 are, for the most part, without strong activating properties. Intact antibodies to acti vating receptors that signal via an immunoreceptor tyrosine-based activating motif (ITAM) also bind to inhibitory Fc receptors, induce coaggregation of the two receptors and ultimately inactivate the cell. If the intact antibodies recognize invariant determinants, then the inhibition is polyclonal. If the antibodies react to variable determinants, such as those within the antigen-binding site, then inactivation is more restricted. Intact antibodies to antigenic determinants also inhibit by Fc-dependent mechanisms; this inhibition is not determinant specific but can involve any other determinants on the antigenic molecule or particle. All these forms of inhibition involve modulation of the positive signal sent through the ITAM. In some cases, polyclonal activation of one cell type inhibits other cell type(s). For example, concanavalin A polyclonally activates T cells, including T cells that suppress B cell responses in a polyclonal fashion.

Lymphocytes undergo explosive expansion in response to antigenic challenge. This provides a basis for active immunity, but presents two problems. How are responses to self antigens controlled? How are a majority of lymphocytes that respond to an antigenic challenge dealt with after the antigenic challenge has been eliminated? Lymphocytes have a range of cell surface molecules which transmit inhibitory signals. Beside the inhibitory Fc receptor, other receptors listed in Table 2 help to keep lymphocyte activity under control. While many of these receptors can, under experimental conditions, inhibit in a polyclonal fashion, under physiologic situations most act in an antigen-specific fashion due to regulation by the antigen receptor.

Polyclonal activators may also cause profound inhibition, an example being superantigens. Such superantigens, for example those derived from Staphylococcus aureus, activate T cells in a polyclonal fashion, but this activation can be followed by deletion of superantigen-binding T cells. This deletion creates holes in the T cell repertoire, potentially reducing the effective number of T cell antigen receptors available in immune responses.

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