Mochizuki M
Department of Ophthalmology, University of Tokyo Branch Hospital, School of Medicine, Japan.
Jpn J Ophthalmol. 1987;31(2):230-4.
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.