title: Contribution of host radioresistant T cells to the clonal elimination of minor lymphocyte stimulatory-1a reactive T cells in mouse bone marrow chimeras.
abstract: When bone marrow (BM) cells from I-E+ and minor lymphocyte stimulatory (Mls) antigen (Ag) disparate mice (Mls-1b) were transplanted to lethally irradiated Mls-1a mice, Mls-1a reactive T cells were found to be completely deleted from the developing thymocyte population in these [Mls-1b-->Mls-1a] radiation chimeras. It has been shown that BM-derived class II (Ia) positive cells play an essential role in this clonal deletion. Thus, Mls-1a Ag appeared to have been transferred from recipient cells to the Ia+ cells derived from donor BM. These Mls-1a-Ia complexes appear to be responsible for elimination of the Mls-1a reactive T cells that have also been derived from donor BM. However, definition of the cells of the recipient that generate the Mls-1a Ag and transfer them to the BM-derived Ia+ cells has remained unclear to date. In the analysis described herein, we have investigated the tolerogenicity of Mls-1a Ag derived from host T cells which represent a major population of radioresistant cells in the [Mls-1b-->Mls-1a] chimeras. When recipient T cells that had been collected and purified from spleens of [Mls-1b-->Mls-1a] chimeras were administered i.v. into [Mls-1b] chimeras, Mls-1a reactive V beta 6+, V beta 8.1+, or V beta 9+ T cells were completely eliminated. Thus, residual radioresistant host T cells present in the radiation BM chimeras are the cells which produce the Mls-1a Ag. These Mls-1a Ags ultimately contribute to the clonal elimination of Mls-1a reactive T cells from the developing thymocyte population. The present findings indicate that recipient T cells which can survive lethal irradiation and produce intrinsic superantigens alter eventually the T cell repertoire in the thymus which have been developing from precursors of donor BM.
authors.affiliation: Institute of Immunological Science, Hokkaido University, Sapporo, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Arase
authors.forename: H
authors.initials: H
authors.lastname: Arase
authors.forename: R A
authors.initials: RA
authors.lastname: Good
authors.forename: K
authors.initials: K
authors.lastname: Onoé
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D016026:Bone Marrow Transplantation / Q000276:immunology*; D017637:Clonal Deletion; D015333:Gene Rearrangement, beta-Chain T-Cell Antigen Receptor; D007108:Immune Tolerance; D051379:Mice; D008806:Mice, Inbred AKR; D008815:Mice, Inbred Strains; D016747:Minor Lymphocyte Stimulatory Antigens / Q000276:immunology*; D011828:Radiation Chimera; D011948:Receptors, Antigen, T-Cell / Q000276:immunology*; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000528:radiation effects
chemical_list: D016747:Minor Lymphocyte Stimulatory Antigens; D011948:Receptors, Antigen, T-Cell