T-lymphocyte and experimental autoimmune uveoretinitis.
The immunopathogenic mechanisms underlying S-antigen-induced experimental autoimmune uveoretinitis (EAU) were discussed with particular emphasis on the cellular immune response on the basis of the following data: 1) athymic nude rats did not develop EAU unless sensitized lymphocytes obtained from heterozygous rats were transferred into the nude rats; 2) cyclosporine, an immunosuppressant selective to the T-lymphocytes, completely inhibited the cellular immune response to S-antigen as well as EAU induction; 3) a lymphocyte population having the capacity to produce interleukin 2 in response to S-antigen appeared prior to the onset of EAU; and 4) EAU was successfully transferred into syngenic animals by sensitized T-lymphocytes or by a T-cell line specific to S-antigen. These data were thought to indicate that the T-lymphocyte or the cellular immune response to S-antigen constitutes the essential factor for the development of EAU.
Mochizuki
M
M
Department of Ophthalmology, University of Tokyo Branch Hospital, School of Medicine, Japan.
D000818:Animals; D000941:Antigens; D019393:Arrestin; D001327:Autoimmune Diseases / Q000139:chemically induced / Q000276:immunology*; D003524:Cyclosporins / Q000494:pharmacology; D005136:Eye Proteins; D007116:Immunization, Passive; D007376:Interleukin-2 / Q000276:immunology; D051381:Rats; D011919:Rats, Inbred Strains; D012173:Retinitis / Q000139:chemically induced / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D014605:Uveitis / Q000139:chemically induced / Q000276:immunology*
D000941:Antigens; D019393:Arrestin; D003524:Cyclosporins; D005136:Eye Proteins; D007376:Interleukin-2