Blackwell Publishing Journal Backfiles 1879-2005
Target of an antiproliferative antibody-1 (TAPA-1/CD81) has been shown to be non-covalently associated to HLA-DR antigens on the cell surface of B cells. In this study the authors report that triggering of CD81 by MoAb 5A6 or 1D6 significantly (P 〈 0.05) up-regulates the release of tumour necrosis factor-α (TNF-α) by the Epstein–Barr virus-positive (EBV)-B lymphoblastoid cell line JY. The accumulation of TNF-α in the culture medium of JY cells incubated with either anti-CD81 MoAb was found to be dose-dependent and similar to that obtained following crosslinking of HLA-DR antigens with MoAb L243. The effect of the combination of anti-CD81 and anti-HLA-DR MoAb on the release of TNF-α by JY cells was not synergistic or additive. In addition, the combination of anti-CD81 and anti-HLA-DR MoAb did not affect proliferation and homotypic aggregation of JY cells induced by each MoAb used alone. Both anti-CD81 or anti-HLA-DR MoAb induced protein tyrosine phosphorylation. However, different cytoplasmic proteins were phosphorylated following triggering of either molecule. Taken together, the data demonstrate that CD81 and HLA-DR antigens induce similar effector phenomena in the regulation of TNF-α release, homotypic aggregation and inhibition of JY cell proliferation.
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