title: A stimulatory Mls-1 superantigen is destroyed by ultraviolet light while other Mtv-7 antigens remain intact. Significance for Mls-1 unresponsiveness.
abstract: Accessory cells present Ag together with costimulatory signals as immunogens and without costimulatory signals as tolerogens. Responsiveness and unresponsiveness are thus alternatives of T cell immune reactions to Ag. Superantigens appear to make an exception; being presented by accessory cells capable of providing costimulatory signals, these Ag induce a strong T cell response but leave T cells unresponsive to a secondary challenge (anergy). We show here that T cell anergy is not a mandatory consequence of superantigen-induced activation. Mls-1- BALB/c recipients of DBA/2 spleen cells mount vigorous Mls-1 responses in vivo but their T cells retain the ability to respond to a subsequent Mls-1 challenge in vitro. We tested the possibility that the inability of DBA/2 spleen cells to inactivate Mls-1-reactive BALB/c T cells was the result of excessive costimulatory activity provided by Mls-1+ DBA/2 B cells. Costimulatory accessory cell activity has been reported to be destroyed by UV light. We exposed superantigen-presenting cells to UV radiation and found that they had lost the ability to stimulate an Mls-1 response without, however, gaining the capacity to render Mls-1-specific T cells anergic. Despite their inability to noticeably stimulate Mls-1-reactive T cells, UV-treated Mls-1+ lymphocytes induced an absolute unresponsiveness in Mls-1- recipients to a second challenge with the superantigen. Our data are in agreement with previous evidence, confirmed here, that BALB/c mice establish immunity against Mls-1+ cells, which causes the accelerated rejection of superantigen-bearing lymphocytes. Thus, our data imply that, whereas it takes stimulatory superantigenic Mtv-7 gene products to induce the activation of superantigen-reactive T cells, nonsuperantigenic Mtv-7 gene products may induce an immune response leading to the elimination of Mtv-7+ lymphoid cells.
authors.affiliation: New York Medical College, Department of Microbiology and Immunology, Valhalla 10595.
authors.forename: G
authors.initials: G
authors.lastname: Dannecker
authors.forename: S
authors.initials: S
authors.lastname: Mecheri
authors.forename: K
authors.initials: K
authors.lastname: Clarke
authors.forename: A
authors.initials: A
authors.lastname: Dudhane
authors.forename: Z Q
authors.initials: ZQ
authors.lastname: Wang
authors.forename: M K
authors.initials: MK
authors.lastname: Hoffmann
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000528:radiation effects*; D001402:B-Lymphocytes / Q000276:immunology / Q000528:radiation effects; D007108:Immune Tolerance; D007156:Immunologic Memory; D008213:Lymphocyte Activation / Q000528:radiation effects; D008324:Mammary Tumor Virus, Mouse / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D016747:Minor Lymphocyte Stimulatory Antigens / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D014466:Ultraviolet Rays
chemical_list: D016747:Minor Lymphocyte Stimulatory Antigens