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Co‐receptor‐independent signal transduction in a mismatched CD8 + major histocompatibility complex class II‐specific allogeneic cytotoxic T lymphocyte
Author(s) -
Eshima Koji,
Tachibana Makoto,
Suzuki Harumi,
Yamazaki Sunao,
Shinohara Nobukata
Publication year - 1997
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.1830270109
Subject(s) - biology , t cell receptor , cytotoxic t cell , cd8 , major histocompatibility complex , microbiology and biotechnology , clone (java method) , t cell , cd3 , t lymphocyte , receptor , lymphokine , antigen , immunology , immune system , biochemistry , gene , in vitro
Abstract The contribution of co‐receptors in signal transduction upon T cell receptor (TCR)‐mediated recognition of major histocompatibility complex (MHC) class II antigen by mature T lymphocytes expressing TCR derived from the apparently co‐receptor‐independent, I‐A k ‐specific allogeneic CD8 + CTL clone QM11 has been examined. Mature double‐negative, CD8 + and CD4 + bulk T cell lines and clones expressing TCR QM11 were developed from TCR QM11 transgenic mice. All these T cells, irrespective of co‐receptor expression, showed specific lytic activity on cells expressing I‐A k . Furthermore, co‐receptorless mutants were obtained from a CD4 + and CD8 + clone. The responses of these co‐receptorless mutants upon specific recognition of the alloantigen, as judged by cytolytic activity, granule exocytosis, lymphokine production, proliferation, and tyrosine phos‐phorylation of the ξ chain, were comparable to those of the original clones. Thus, the results proved the co‐receptor independence of the recognition of I‐A k by TCR QM11 and further indicated there is no indispensable unique signal transduced by co‐receptors. However, when the amount of the available antigen was limited by anti‐I‐A k antibody, the CD4 + T cell clone showed a remarkable resistance to the inhibition whereas the mismatched CD8 + clone was readily inhibitable. The anti‐I‐A k ‐resistant component of the CD4 + clone showed dependency on the CD4 molecule. Taken collectively, the results indicate that the role played by a co‐receptor molecule in mature T cells is purely quantitative amplification of the signal through the formation of a TCR/MHC/co‐receptor ternary complex, and also indicate that the role of co‐receptor molecules as TCR‐independent adhesion molecules is at best minimal.