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CD82, tetra‐span‐transmembrane protein, is a regulated transducing molecule on U937 monocytic cell line
Author(s) -
LebelBinay Sophie,
Lagaudrière Cécile,
Fradelizi Didier,
Conjeaud Hélène
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.57.6.956
Subject(s) - biology , microbiology and biotechnology , cell surface receptor , calcium in biology , u937 cell , intracellular , signal transduction , receptor , cell culture , biochemistry , genetics
The mononuclear cell surface protein IA4, recently classified as CD82, was originally identified in our laboratory by the IA4 monoclonal antibody (mAb), because of its high expression on three lymphoblastoid, LAK‐susceptible, variant cell lines. We have characterized CD82 as a new activation/differentiation marker of mononuclear cells. This protein belongs to the new family of TST proteins (tetra spans transmembrane), which includes CD9, CD37, CD53, CD63, and CD81 (TAPA‐1). Here we demonstrate that cross‐linking of IA4 mAbs induces an increase of intracellular free calcium in U937 cells and tyrosine phosphorylation of various proteins. Our data indicate that the intracellular calcium increase is initiated by a phospholipase C (PLC)–induced PtdIns(l,4,5)P 3 second messenger followed by a more stable change, linked to extracellular calcium entry. This transducing signal was dependent on dual engagement of both CD82 and Fc receptors. Surface cross‐linking of CD82 together with Fc receptors (FcRs) induces a specific long‐lasting increase of intracellular calcium, whereas FcR cross‐linking alone induces only a transient calcium mobilization. These results suggest that, upon cross‐linking of CD82, a multimolecular complex including CD82 and FcR could be induced that is able to trigger signal transduction. We have previously shown that CD82 membrane expression is up‐regulated during differentiation of human monocytes. Using U937 cells, we demonstrate here that several cytokines [interleukin‐1β (IL‐lβ), IL‐4, IL‐6, IL‐13, interferon‐γ, tumor necrosis factor α] could significantly up‐regulate the surface expression of CD82 antigen, by contrast with FcR surface expression, which was up‐regulated only after IFN‐γ treatments. Based on our finding of a strict dependence of CD82 activation on FcR stimulation, we suggest a putative role of CD82 in enhancing FcR‐mediated activation of cells from the monocyte/macrophage lineage. J. Leukoc. Biol. 57: 956–963; 1995.