Effect of tumor necrosis factor alpha on mitogen-activated human B cells.
In this study we demonstrate that the monocyte/macrophage product, tumor necrosis factor alpha (TNF-alpha), has significant in vitro effects of B cell function. It costimulated with anti-mu in the induction of B cell DNA synthesis, and it prolonged the DNA synthesis initiated in B cell cultures stimulated with the human B cell mitogen, Staphylococcus aureus Cowan strain I (SAC). The addition of either IL-1 or IFN-gamma to TNF-alpha resulted in a substantial further increase in DNA synthesis. The addition of TNF-alpha to IL-2, a known inducer of SAC-activated B cell Ig secretion, resulted in a twofold enhancement in the amount of IL-2 stimulated B cell Ig secretion. Receptor binding studies with 125I-TNF-alpha demonstrate a marked increase in TNF-alpha binding sites after B cell activation (approximately 6,000 sites per cell, with an apparent Kd of 2.0 X 10(-10) M). Thus, TNF-alpha may be an important factor in human B cell function and is likely to interact with other T cell and monocyte derived cytokines in the regulation of human B cell proliferation and Ig production.
D001402:B-Lymphocytes / Q000187:drug effects / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D004247:DNA / Q000096:biosynthesis; D006023:Glycoproteins / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D007075:Immunoglobulin M / Q000096:biosynthesis; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000502:physiology; D007376:Interleukin-2 / Q000502:physiology; D008213:Lymphocyte Activation / Q000187:drug effects*; D011956:Receptors, Cell Surface / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha
D006023:Glycoproteins; D007075:Immunoglobulin M; D007375:Interleukin-1; D007376:Interleukin-2; D011956:Receptors, Cell Surface; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D004247:DNA