ArticleClinical and experimental immunology1999
Apoptosis of CD4+ T cells occurs in experimental autoimmune anterior uveitis (EAAU).
Article in Clinical and experimental immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- Chemotherapy of breast cancer cells alters susceptibility to complement-mediated opsonization and killing.Medical oncology (Northwood, London, England) · 2025Article
- Levels of thrombopoietin in aqueous humor of patients with noninfectious acute anterior uveitis.Clinical ophthalmology (Auckland, N.Z.) · 2015Article
- Expressions of lymphotactin and its receptor, XCR, in Lewis rats with experimental autoimmune anterior uveitis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2010Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the spontaneous turning off mechanism of endogenous uveitis, EAAU was induced in Lewis rats. Immunohistochemical and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) stains revealed that CD4+ T cells were predominant in the uveal tissue of EAAU and that the apoptosis of these cells had occurred and progressed throughout the inflammatory period in EAAU eyes. The immunohistochemistry and in situ hybridization for Fas ligand (FasL) expression showed that the expression of Fas ligand was increased in the EAAU eyes compared with control eyes. These results suggest that the apoptosis of CD4+ T cells may play a key role in the spontaneous turning off mechanism of intra-ocular inflammation and that the induction of apoptosis may be mediated by the Fas-FasL system in EAAU.
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