T-cell-derived factor B151-TRF1 IL-5 activates blastoid cells among unprimed B cells to induce a polyclonal differentiation into immunoglobulin M-secreting cells.

Two distinct murine B-cell differentiation factors, designated B 151 -TRY 1 and B 151-TRF2, were described originally as B151 K12 T-cell hybridoma-derived lymphokines that induce immunoglobulin (Ig) secretion by antigen-activated B cells and unstimulated B cells, respectively. In the present study, we found that a highly purified B1 51-TRF1 fraction prepared by reversed-phase high-performance liquid chromatography (RP-H PLC) also has the ability to cause a polyclonal differentiation of unstimulated B cells into IgM-secreting cells in the apparent absence of co- stimulant. The activity of the B151-TRF1 fraction but not the B151-TRF2 fraction on unstimulated B cells was markedly inhibited by addition of a monoclonal antibody (mAb) specific for the B151- TRF 1/IL-S to the culture. To determine whether 8151 -TRF 1/IL-S and 8151 -TRF2 act on distinct populations among unstimulated B cells, the responsiveness of neonatal B cells and adult B cells that had been fractionated by Percoll density gradient centrifugation was assessed. B15 l-TRFI/IL-5 predominantly acted on lower density B cells, which appeared around 3 weeks after birth in the spleen. In contrast, B151-TRF2 could activate both lower and higher density B cells almost equally and B 151 -TRF2-responsive B cells were already present by 1 week of age. Thus, these results suggest that B151-TRFI/IL-5 and B151-TRF2 act on distinct subpopulations among antigen-unprimed normal B cells to induce IgM-secreting cells. [ABSTRACT FROM AUTHOR]