title: Differential susceptibility of cells expressing allogeneic MHC or viral antigen to killing by antigen-specific CTL.
abstract: CD8(+) cytotoxic T lymphocytes (CTLs) generated by immunization with allogeneic cells or viral infection are able to lyse allogeneic or virally infected in vitro cells (e.g., lymphoma and mastocytoma). In contrast, it is reported that CD8(+) T cells are not essential for allograft rejection (e.g., heart and skin), and that clearance of influenza or the Sendai virus from virus-infected respiratory epithelium is normal or only slightly delayed after a primary viral challenge of CD8-knockout mice. To address this controversy, we generated H-2(d)-specific CD8(+) CTLs by a mixed lymphocyte culture and examined the susceptibility of a panel of H-2(d) cells to CTL lysis. KLN205 squamous cell carcinoma, Meth A fibrosarcoma, and BALB/c skin components were found to be resistant to CTL-mediated lysis. This resistance did not appear to be related to a reduced expression of MHC class I molecules, and all these cells could block the recognition of H-2(d) targets by CTLs in cold target inhibition assays. We extended our observation by persistently infecting the same panel of cell lines with defective-interfering Sendai virus particles. The Meth A and KLN205 lines infected with a variant Sendai virus were resistant to lysis by Sendai virus-specific CTLs. The Sendai virus-infected Meth A and KLN205 lines were able to block the lysis of Sendai virus-infected targets by CTLs in cold target inhibition assays. Taken together, these results suggest that not all in vivo tissues may be sensitive to CTL lysis.
authors.affiliation: Department of Physiology, Osaka Medical College, Takatsuki, Osaka, Japan.
authors.forename: Koutetsu
authors.initials: K
authors.lastname: Lee
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Takenaka
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yoneda
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Goto
authors.forename: Kouichi
authors.initials: K
authors.lastname: Sano
authors.forename: Mahito
authors.initials: M
authors.lastname: Nakanishi
authors.forename: Akiko
authors.initials: A
authors.lastname: Eguchi
authors.forename: Masashi
authors.initials: M
authors.lastname: Okada
authors.forename: Junko
authors.initials: J
authors.lastname: Tashiro
authors.forename: Kanji
authors.initials: K
authors.lastname: Sakurai
authors.forename: Takahiro
authors.initials: T
authors.lastname: Kubota
authors.forename: Ryotaro
authors.initials: R
authors.lastname: Yoshida
mesh_terms: D000818:Animals; D000956:Antigens, Viral / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002294:Carcinoma, Squamous Cell / Q000276:immunology; D002460:Cell Line; D045744:Cell Line, Tumor; D003601:Cytotoxicity Tests, Immunologic; D003602:Cytotoxicity, Immunologic / Q000276:immunology*; D003673:Defective Viruses / Q000276:immunology; D005354:Fibrosarcoma / Q000276:immunology; D006183:H-2 Antigens / Q000276:immunology*; D006649:Histocompatibility Antigens; D015395:Histocompatibility Antigens Class I / Q000276:immunology; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D012327:RNA Virus Infections / Q000276:immunology; D029082:Sendai virus / Q000276:immunology*; D012867:Skin / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*
chemical_list: D000956:Antigens, Viral; D006183:H-2 Antigens; D006649:Histocompatibility Antigens; D015395:Histocompatibility Antigens Class I