title: T cell clones are killed by a thymic stromal cell monolayer following stimulation of T cell receptor with antigen and/or H-2 molecules on the monolayer.
abstract: A thymic stromal cell clone, MRL104.8a, expressed class I and class II H-2k antigens after exposure to gamma-interferon (gamma-IFN) and produced thymic stroma-derived T cell growth factor (TSTGF) irrespective of gamma-IFN exposure. Culturing the keyhole limpet hemocyanin (KLH)-specific, I-Ek-restricted 9-16 helper T cell (Th) clone on an Ia (I-Ak and I-Ek)-expressing MRL 104.8a monolayer induced potent proliferation of the 9-16 cells by virtue of the TSTGF produced by the monolayer. In contrast, the addition of KLH to cultures resulted in lethal growth inhibition of the 9-16 Th clone. Such a phenomenon was also observed for various Th as well as cytotoxic T lymphocyte (CTL) clones, and the following were revealed: (i) the growth of the ovalbumin (OVA)-or bovine thyroglobulin (BTg)-specific Th clone on the la-expressing MRL 104.8a monolayer was also inhibited by addition of the relevant antigen. The fact that these Th clones required antigen-presenting cells (APC) capable of processing antigen for the recognition of the respective target antigen suggested the potential of MRL 104.8a cells for antigen-processing; (ii) the lethal growth inhibition of KLH-specific, I-Ak (23-1-8)- or I-Ek (9-16)-restricted Th clone was prevented selectively by anti-I-Ak or anti-I-Ek antibody respectively; (iii) the I-Ek-alloreactive Th clone (2-13) was supported for its growth on a gamma-IFN-unexposed MRL 104.8a monolayer, whereas this clone was killed on an I-Ek-expressing monolayer; and (iv) when I-Ak-reactive CTL clones were cultured on an Ia- or Ia+ monolayer, CTL clones failed to exhibit cytotoxic effect on either the Ia- or the Ia+ monolayer, but were conversely killed by the Ia+ monolayer. Its killing was also prevented by an antibody which inhibits the recognition of Ia antigen on the monolayer by CTL clones.(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Biomedical Research Center, Osaka University Medical School, Japan.
authors: H
authors: H
authors: Matsubara
authors: H
authors: H
authors: Kosaka
authors: S
authors: S
authors: Sogo
authors: S
authors: S
authors: Maruo
authors: S
authors: S
authors: Sugihara
authors: Y
authors: Y
authors: Asano
authors: Y
authors: Y
authors: Kohno
authors: M
authors: M
authors: Kimoto
authors: G
authors: G
authors: Suzuki
authors: K
authors: K
authors: Ishimura
mesh_terms: D000818:Animals; D000941:Antigens; D002999:Clone Cells / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D006183:H-2 Antigens; D006433:Hemocyanins / Q000276:immunology; D008854:Microscopy, Electron; D011948:Receptors, Antigen, T-Cell; D013601:T-Lymphocytes / Q000276:immunology* / Q000648:ultrastructure; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
chemical_list: D000941:Antigens; D006183:H-2 Antigens; D011948:Receptors, Antigen, T-Cell; D006433:Hemocyanins; C032808:keyhole-limpet hemocyanin