A noncognate interaction with anti‐receptor antibody‐activated helper T cells induces small resting murine B cells to proliferate and to secrete antibody

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Abstract
Culture of small resting allogeneic B cells (of an irrelevant haplotype) with two clones of T helper (Th) cells that were activated by the F23.1 anti‐T cell receptor antibody led to the activation of B cells to proliferate and to secrete antibody. Th cell supernatants by themselves had no effect on resting B cells (even in the presence of intact F23.1 antibody), but could induce antibody secretion by anti‐Ig‐preactivated B cells. Both F23.1‐1 clones (E9.D4 and 4.35F2) and one F23.1‐ clone (D2.2) could synergize with supernatants from activated E9.D4 T cells to induce B cell activation. F(ab'), fragments of F23.1 induced E9.D4 to activate B cells as efficiently as intact F23.1, and B cell populations that had been incubated with F23.1 were not activated when cultured with E9.D4, although T cells recognized cell‐presented F23.1 and were weakly activated. Reduction of the density of F23.1 adsorbed to plastic resulted in weak T cell activation, and these T cells did not induce B cell responses. Haptenated B cell populations, although recognized by E9.D4, were not activated. Separation of T and B cells by a 0.4‐μm membrane prevented T‐dependent B cell activation, although Th cell‐derived B cell‐activating lymphokines would be assayed across these membranes. These results suggest a polyclonal noncognate B cell activation that depends on physical contact between B cells and activated T cells. The requirement for a cognate interaction of Th with B cells for the production and delivery of B help can therefore be overcome by activating Th cells with high densities of T cell receptor ligands.