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MHC Class II expression in the retina during experimental autoimmune uveitis
Author(s) -
LIPSKI D,
DEWISPELAERE R,
FOUCART V,
CASPERS L,
BRUYNS C,
WILLERMAIN F
Publication year - 2014
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2014.t056.x
Subject(s) - cd31 , mhc class ii , uveitis , biology , retina , pathology , cd40 , immunology , antigen , medicine , in vitro , immunohistochemistry , cytotoxic t cell , major histocompatibility complex , biochemistry , neuroscience
Purpose Autoimmune posterior non infectious uveitis induction requires intraocular MHCII‐dependent recognition of a retinal antigen by autoreactive T cells. MHCII basal retinal expression is weak, but possibly induced during uveitis. In this work, we aim to identify the retinal cell types susceptible to express MHCII during EAU. Methods C57Bl/6 mice were immunized with IRBP1–20. At day 12, T cells were semi‐purified from lymph nodes and spleens, re‐stimulated in vitro and injected to naive C57Bl/6 mice. Fundoscopy was performed after 3 weeks. MHCII expression was analyzed by immunofluorescence on eye cryosections and co‐labellings for GFAP, CD31, endoglin and IBA‐1 realized to identify cells expressing MHCII. Results No expression of MHCII is detected in naive retinas, while strong induction is found during EAU. The majority of cells infiltrating the vitreous co‐stain for MHCII and IBA‐1, a marker of macrophages and microglial cells. Extravasated cells around vasculitis lesions also show MHCII staining, partially co‐localized with IBA‐1. At the vascular level, marginal expression of MHCII appears on GFAP+ (glial and Müller cells) and CD31+ (endothelial cells, platelets and macrophages) cells, while no co‐staining is observed with endoglin. MHCII is expressed on the ciliary body epithelium and lightly on the RPE. Microglia displays an intense diffuse MHCII expression. Conclusion Our results support a strong MHCII induction during EAU, on both retinal and infiltrating cells. At the level of the BRB, although RPE cells express some MHCII, our data do not demonstrate expression of MHCII by endothelial cells. The question of how antigen presentation to activated T cells occurs at the site of the inner BRB remains to be addressed.