title: Responsiveness of T cells to mutant major histocompatibility complex class I antigen. II. Role of stimulator-type accessory cells with reference to interleukin 1 production.
abstract: Mechanisms of the activation of T cells responding to major histocompatibility complex (MHC) class I antigen were investigated with special reference to interleukin 1 (IL-1) production from stimulator-type accessory cells. For this purpose, we used mainly fractionated Lyt-2+T cells of C57BL/6 (B6) mice as responder cells and irradiated spleen cells or those deprived of adherent cells of B6.C-H-2bm1 (bm1) mice as stimulator cells. Lyt-2+ T cells of B6 mice proliferated in the presence of irradiated whole spleen cells of bm1 mice but did not to Sephadex G-10 column-passed bm1 spleen cells. The unresponsiveness in the latter case was overcome by the supplement of recombinant IL-1 and/or IL-2 in the culture medium. These interleukins were shown to promote the proliferative response of B6 Lyt-2+ T cells in the presence of stimulator-type T or B cells. Both interleukins also facilitated the generation of cytotoxic T cells from B6 Lyt-2+ cells to H-2Kbm1 antigen in the mixed lymphocyte culture deficient in stimulator-type accessory cells. IL-1 was shown to enhance the expression of IL-2 receptor on the responding Lyt-2+ T cells as assessed by flow cytometry. IL-1 binding to responding T cells were also assayed by means of iodinated IL-1 and was shown to increase significantly on responding Lyt-2+ cells. Overall results indicate that accessory cells might play dual roles in the activation of Lyt-2+ T cells responding to allogeneic MHC class I antigen: direct presentation of the antigen to responder T cells and production of IL-1. Both signals are essentially required for Lyt-2+ T cells responding to allogeneic MHC class I antigen to initiate proliferation and also to differentiate into cytotoxic T cells.
authors.affiliation: Laboratory of Immunology, Niigata University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Saitoh
authors.forename: M
authors.initials: M
authors.lastname: Fujiwara
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000145:classification / Q000276:immunology / Q000378:metabolism*; D000950:Antigens, Ly; D003602:Cytotoxicity, Immunologic; D006183:H-2 Antigens / Q000235:genetics* / Q000276:immunology; D007375:Interleukin-1 / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010641:Phenotype; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology* / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology
chemical_list: D000950:Antigens, Ly; D006183:H-2 Antigens; D007375:Interleukin-1; D015375:Receptors, Interleukin-2