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.
Zola
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Department of Clinical Immunology, Flinders Medical Centre, South Australia.
Nikoloutsopoulos
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D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000502:physiology; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects*; D010641:Phenotype; D011994:Recombinant Proteins / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D011994:Recombinant Proteins; D014409:Tumor Necrosis Factor-alpha