title: I-J as a second T cell receptor for self--molecular polymorphism and the role in suppressive signal transduction.
abstract: 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.
authors: Department of Immunology, Faculty of Medicine, University of Tokyo, Japan.
authors: T
authors: T
authors: Tada
authors: T
authors: T
authors: Nakayama
authors: Y
authors: Y
authors: Asano
authors: H
authors: H
authors: Kishimoto
authors: K
authors: K
authors: Sano
mesh_terms: D000818:Animals; D004591:Electrophoresis, Polyacrylamide Gel; D000939:Epitopes / Q000032:analysis*; D007519:Isoantigens / Q000032:analysis / Q000502:physiology*; D051379:Mice; D011110:Polymorphism, Genetic; D011948:Receptors, Antigen, T-Cell / Q000502:physiology*; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000939:Epitopes; D007519:Isoantigens; D011948:Receptors, Antigen, T-Cell