Th17 cells play a central role in experimental Candida albican keratitis in mice (99.32)

Abstract

Abstract Our previous studies showed that experimental Candida albican keratitis (CaK) induced an adaptive immune response. Here we explored the role of T lymphocytes in the progress of CaK. Balb/c mice and nude mice on Balb/c background were used for CaK model. CaK was induced by intrastromal injection of Candida albicans spores into the corneas. Keratitis was measured by scoring the lesions. One day before CaK induction, unsorted splenocytes or purified T cells from either Balb/c, C57BL/6 or OVA-TCR Tg DO11.10 mice were adoptively transferred into nude mice, or various T cell subtypes were depleted in Balb/c mice using specific antibodies. We found that, upon challenge with same amount of fungal spores, Balb/c mice developed typical CaK, but nude mice did not show any sign of CaK. Reconstitution of nude mice with either splenocytes or purified T cells built sensitivity of nude mice to CaK induction in a way dependent of numbers but not of MHC- nor TCR-restriction of transferred cells. Depleting Th17 cells with anti-IL17 or anti-IL23 antibodies completely abrogated the capability of Balb/c mice to develop CaK. But depleting Treg cells with anti-CD25 or γδT cells with anti-γδ antibody did not show any effect. Th17 depleted mice did not set up immunological memory either after primary CaK. We conclude that a minimum of Th17 cells are essential in the initiation of fungal keratitis, and T cells play a dual role in the pathogenesis and prognosis of fungal keratitis.