Effect of recombinant human tumour necrosis factor beta (TNF beta) on activation, proliferation and differentiation of human B lymphocytes

Activation, proliferation and differentiation of B lymphocytes are processes controlled by T cells, and the control is mediated in part by the action of lymphokines derived from T cells. In this study we have examined the ability of tumour necrosis factor-beta (TNF beta), a T-cell product, to induce a state of activation in resting B cells, to induce proliferation of already activated B cells, and to stimulate differentiation. Recombinant tumour necrosis factor beta (rTNF beta) was used alone and in conjunction with known stimulators. As judged by several markers of activation (CD23, CDw40, LFA-1, 4F2, MHC class I and class II), rTNF beta did not contribute to the activation of resting B cells, either alone or in conjunction with anti-IgM and IL-4. However, the activation marker detected by the monoclonal antibody Leu 21 did show a greater degree of up-regulation by anti-IgM + IL-4 + rTNF beta when compared with anti-IgM + IL-4. rTNF beta induced proliferation of B cells, but only if activating stimuli were also present. Two other factors which induce proliferation of activated B cells, low molecular weight B-cell growth factor (LMW-BCGF) and IL-2, showed additive effects with rTNF beta. No evidence of changes in differentiation status of the B cells was seen.