Autocrine B-cell stimulation by interleukin-2 during a cognate interaction with T-cells

Interleukin-2 (IL-2) secretion as well as expression of IL-2 receptor has been demonstrated for B-cells in response to several activating stimuli. However, the exact role of B-cell-derived IL-2 in the T-cell-dependent antibody response remains to be determined. Here, we have examined the autocrine regulatory roles of IL-2 secreted from B-cells. Splenic resting B-cells were stimulated with a fixed pre-activated Th1 clone, G1.19, in the presence of a single amino acid-substituted peptide (pD129A; Ala-129 substituted for Asp-129), an analog of the original ligand (p119-133, derived from bovine beta-lactoglobulin) recognized by G1.19 cells. pD129A allowed a cognate interaction between B-cells and fixed pre-activated G1.19 T-cells, but pD129A had no agonistic activity against G1.19 T-cells. Thus, the level of expression of B-cell-activating molecules on T-cells remained unchanged after stimulation with pD129A. Regardless of the lack of ability to induce IL-2 secretion in the case of T-cells, pD129A significantly enhanced antibody secretion from B-cells, and this was partially blocked by anti-IL-2 antibody. Furthermore, IL-2 secretion from B-cells was modestly upregulated in response to added pD129A. Taken together, these data suggest that helper signals from interacting cognate T-cells induce IL-2 secretion by B-cells, which can enhance antibody secretion in an autocrine manner.