We shall continue our investigation of the role of lymphokines in the activation of B cells. Interleukin 1 (IL-1) has traditionally been the focus of our lymphokine studies; it conditions B cells to differentiate into antibody-producing cells when intracellular cAMP levels are elevated. We propose that TRF (or interferon) is a factor which controls intracellular cAMP levels and thus B-cell differentiation. B-cell proliferation, through which antigen-reactive B cells increase their clone size, is controlled by interleukin-2 (IL-2). We propose further that IL-2 helps B cells sustain cell division after they receive proliferative stimulus from antigen; IL-2 curbs an intracellular (cAMP-mediated) mechanism which turns proliferation off. T cell- and macrophage-derived lymphokines are released as a consequence of MHC-restricted interaction between T cells and macrophages. The T cell recognizes in this interaction foreign antigen as well as MHC antigen on the macrophage surface. We propose that the T-cell receptor recognizes both antigens in unmodified form and that foreign antigen facilitates the interaction of the T-cell receptor with MHC antigen as a consequence of which effector function (e.g., release of IL-1 and IL-2) ensues. This process does not occur spontaneously, because T cells and macrophages mask receptor and MHC antigen with charged carbohydrates. Removal of these charged molecules from cell surfaces initiates polyclonal T-cell and macrophage-effector function. (HF)
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