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I-J as a second T cell receptor for self--molecular polymorphism and the role in suppressive signal transduction
1Department of Immunology, Faculty of Medicine, University of Tokyo, Japan.
We have been able to demonstrate an I-J epitope on the cell surface of interleukin 2 (IL-2) dependent T cell clones of both T helper (Th) and suppressor T cells (Ts) lineages by flow microfluorometry with fluoresceinated anti-I-Jk, and to identify the molecule by the specific immunoprecipitation and the gel analysis. The I-J molecule thus detected is a novel 90K dimeric molecule composed of 45K glycopeptide subunits distinct from conventional T cell receptor (TcR) or CD28. The molecule is not comodulated with TcR or T3 on the cell surface. Monoclonal anti-I-J can inhibit various major histocompatibility complex (MHC)-restricted T cell functions including Ca2+ influx, antigen-induced T cell proliferation and IL-2 production, indicating that the ligation of I-J molecules results in a negative signal transduction. Since it has been reported that the I-J phenotype undergoes a systematic adaptive alteration in radiation bone marrow chimeras in association with the acquired class II restriction, it is likely that I-J is a novel receptor for self MHC apart from TcR heterodimer and is required for a negative signal transduction.
We have been able to demonstrate an I-J epitope on the cell surface of interleukin 2 (IL-2) dependent T cell clones of both T helper (Th) and suppressor T cells (Ts) lineages by flow microfluorometry with fluoresceinated anti-I-Jk, and to identify the molecule by the specific immunoprecipitation and the gel analysis. The I-J molecule thus detected is a novel 90K dimeric molecule composed of 45K glycopeptide subunits distinct from conventional T cell receptor (TcR) or CD28. The molecule is not comodulated with TcR or T3 on the cell surface. Monoclonal anti-I-J can inhibit various major histocompatibility complex (MHC)-restricted T cell functions including Ca2+ influx, antigen-induced T cell proliferation and IL-2 production, indicating that the ligation of I-J molecules results in a negative signal transduction. Since it has been reported that the I-J phenotype undergoes a systematic adaptive alteration in radiation bone marrow chimeras in association with the acquired class II restriction, it is likely that I-J is a novel receptor for self MHC apart from TcR heterodimer and is required for a negative signal transduction.