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Induction of T cell function via the gp33/27 activation inducer molecule (AIM) requires co‐expression of the CD3/TcR complex
Author(s) -
Rincón Mercedes,
Cebrián Marta,
SánchezMadrid Francisco,
LópezBotet Miguel
Publication year - 1989
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830190528
Subject(s) - t cell receptor , jurkat cells , cd3 , biology , t cell , microbiology and biotechnology , monoclonal antibody , inducer , interleukin 2 , t lymphocyte , signal transduction , receptor , antigen , antibody , immunology , biochemistry , immune system , cd8 , gene
Abstract Monoclonal antibodies specific for a dimeric cell surface activation antigen (gp33/27), preliminary designated as activation inducer molecule (AIM), are capable of triggering interleukin 2 (IL 2) synthesis, IL 2 receptor expression and T cell proliferation when used in conjunction with phorbol esters. We have analyzed the functional relationship between the AIM and the CD3/TcR‐mediated activation pathways. Transient modulation of the CD3/TcR complex in the Jurkat cell line, as well as the stable loss of the CD3/TcR surface expression in variant subclones, determined an inhibition of the IL 2 production triggered by anti‐AIM monoclonal antibody (mAb). In contrast, neither the surface expression of AIM nor the ability to respond to a Ca 2+ ionophore were affected. Similar results were observed in peripheral blood T lymphocytes, detecting after CD3 modulation an inhibition of both the IL 2 synthesis and the proliferative response to anti‐AIM mAb. Altogether our data indicate that the activation pathway triggered by anti‐AIM mAb is functionally linked to the expression of the CD3/TcR complex in mature T cells.