Production of tumor necrosis factor/cachectin by human B cell lines and tonsillar B cells.

Abstract

The production of TNF/cachectin by human B cell lines and tonsillar B cells was examined. Of the 15 B cell lines examined, 9 cell lines synthesize TNF mRNA constitutively. PMA stimulated most cell lines to accumulate increased amounts of TNF. SeD, 8866P, 32al, RPMI 1788, and four bone marrow-derived EBV-transformed cell lines accumulated high levels of TNF mRNA when stimulated by PMA. TNF production by these cell lines was examined. RPMI 1788 and WIH8 produced little TNF constitutively, but synthesized 5-7 ng/ml TNF when stimulated by PMA. A pre-B cell line, Nalm-6, did not synthesize any detectable amount of TNF mRNA, even with PMA stimulation. Tonsillar B cells could also be stimulated to produce TNF. PMA or Staphylococcus aureus Cowan I strain (SAC) alone stimulated some TNF mRNA accumulation, whereas B cell growth factor (BCGF) or anti-mu did not. This accumulation was synergistically elevated by the combinations of PMA and SAC, or PMA and anti-mu. BCGF increased PMA-, SAC-, PMA plus SAC-, or PMA plus anti-mu-induced TNF mRNA accumulations about twofold. The accumulation of TNF mRNA in tonsillar B cells stimulated by PMA plus SAC was between 32 and 48 h, the same peak interval as the accumulation of TNF and IL-2 mRNA in tonsillar T cells. This is in contrast to PMA or PMA plus A23187-stimulated RPMI 1788 cells in which TNF mRNA accumulation was maximal at 1-2 h. TNF activities found in tonsillar B cell supernatants correlated with the TNF mRNA levels in the cells. However, more TNF activity was found on the second-day than the third-day supernatants, indicating active TNF uptake by the B cells. Cyclosporin A (CsA) inhibited SAC and anti-mu responses in B cells in much the same way as the anti-CD3 responses in T cells. SAC-, PMA plus SAC-, and PMA plus anti-mu-stimulated, but not PMA-stimulated, increases in TNF mRNA accumulations in tonsillar B cells were inhibited by CsA. TNF production seems to increase in parallel with B cell proliferation, but the relationship of these two functions needs to be further examined.

Mucosal Inducible NO Synthase–Producing IgA+ Plasma Cells in Helicobacter pylori–Infected Patients

“…According to previous studies, EBV transformation of primary human B cells changes various cellular properties (23,24), such as the expression of the cell activation-associated Ag CD38 (25), and the expression of iNOS (26). Furthermore, B-LCLs have been described as expressing various cytokines with a high degree of heterogeneity (24,(27)(28)(29)(30)(31)(32). In our B-LCL, iNOS expression was detectable in highly activated CD38 ++ EBV-infected B cells, but not in CD38 + or CD38 2 B cells (Fig.…”

Tumour necrosis factor: a cytokine with multiple biological activities

“…In fact, although the major source of this cytokine is macrophages (Beutler & Cerami, 1987;Aggarwel et al, 1985), the molecule can also be released by other cell types. These include monocytes stimulated by gamma interferon (Beutler & Cerami, 1987), T lymphocytes and T cell lines following stimulation with phorbol esters and anti-CD3 antibodies in different combinations (Granger & Williams, 1968;Cutri et al, 1987;Scheurich et al, 1987;Sung et al, 1988a;Turner et al, 1987), B lymphocytes (Williamson et al, 1983;Sung et al, 1988b), large granular lymphocytes (Ostensen et al, 1987;Peters et al, 1986) and mast cells (Young et al, 1987).…”

Deficient Priming Activity of Newborn Cord Blood–Derived Polymorphonuclear Neutrophilic Granulocytes with Lipopolysaccharide and Tumor Necrosis Factor-α Triggered with Formyl-Methionyl-Leucyl-Phenylalanine

“…It is now known that TNF-a has diverse physiologic effects and is produced by various cell types and stimuli (18)(19)(20)(21)(22). It has been implicated as an endogenous inflammatory mediator induced by LPS (18,(22)(23)(24) or other bacterial products (I 7).…”