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Triggering of Target of an Antiproliferative Antibody‐1 (TAPA‐1/CD81) Up‐Regulates the Release of Tumour Necrosis Factor‐α by the EBV‐B Lymphoblastoid Cell Line JY
Author(s) -
ALTOMONTE M.,
MONTAGNER R.,
PUCILLO C.,
MAIO M.
Publication year - 1996
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1996.d01-64.x
Subject(s) - antigen , microbiology and biotechnology , lymphoblast , tumor necrosis factor alpha , tyrosine phosphorylation , antibody , cell culture , biology , chemistry , immunology , phosphorylation , genetics
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.