Regulation of rat B cell responses by T cell subsets and interleukin 2.

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Abstract
T cell and interleukin 2 (IL 2) regulation of two phases of B cell activation, 3H-TdR uptake and differentiation to antibody-forming cells, were examined. Monoclonal antibody specific for rat kappa light chains (Mab alpha K) stimulated 3H-TdR uptake in vitro in B cell fractions of Lewis spleen cell populations in the presence of T cells and macrophages (M phi); IL 2 reconstituted the response in enriched B cell cultures depleted of T cells and M phi. When IL 2 was added to primary in vitro cultures, spleen cells yielded 100 to 400 anti-SRBC PFC/culture; no PFC were recorded in the absence of IL 2. These results suggested that IL 2 served as a " second signal" for activation in responsive B cell populations. When monoclonal antibody specific for the W3/25+ T cell subset (Mab W3/25) was incorporated into the assay system, both 3H-TdR uptake and PFC responses were inhibited. IL 2 enhancement of B cell responses or responses of reconstituted B cell and T cell fractions was eliminated in the presence of Mab W3/25, indicating that IL 2 mediation of B cell responses was due in part to participation of W3/25+ T cell helper function. In contrast, monoclonal antibody directed to the OX8-bearing T cells (Mab OX8) had no effect on B cell responses. W3/25+ T cells provided helper activity in the generation of a PFC response, whereas OX8+ cells suppressed the antibody response. W3/25+ T cells responded to antigenic stimuli in the presence of IL 2 by undergoing increased blast transformation. OX8+ cells did not exhibit any response. These data define a regulatory network by which T cells, IL 2, and B cells interact to produce in vitro DNA synthesis and antibody formation in activated rat B cells.