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- W4313368802 abstract "Abstract Autoimmune diseases of the CNS, experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune uveoretinitis (EAU) can be induced by adoptive transfer (AT) of activated brain- or retina-specific T cells. The transferred T cells rest for several days in the recipient’s spleen or lungs, where they proliferate and differentiate to a migratory phenotype before invading the CNS, a process termed “licensing” for pathogenicity (PMID: 27986906). Our previous data in a spontaneous uveitis model in R161H mice bearing a retina-specific TCR indicated that the gut may serve as a priming site for uveitogenic T cells through molecular mimicry of gut flora (PMID: 26238373). We now asked if the gut might also serve as a licensing site for autopathogenic T cells. Naive B10.RIII mice received AT of allotype-marked, activated R161H T cells and were monitored for EAU. Donor cells in tissues were detected by flow cytometry. Three days after AT, donor T cells could be detected in spleen, lung and gut, including the mesenteric lymph nodes and lamina propria of the large and small intestine. Similarly to lung and spleen, R161H T cells in the gut showed signs of proliferation by CFSE dilution. This was not altered by antibiotic treatment of recipients before AT to eliminate gut flora, suggesting that microbiota is not needed to retain effector T cells in the gut. We hypothesize that primed retina-specific T cells can receive licensing signals in the gut. Since in spontaneous uveitis they may also be primed there, this could be of relevance to a disease situation. Further characterization of phenotypic and transcriptomic changes of “licensed” R161H cells retrieved from the gut may help to elucidate the local signals important for licensing at this site." @default.
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- W4313368802 date "2020-05-01" @default.
- W4313368802 modified "2023-09-25" @default.
- W4313368802 title "The gut as a potential licensing site for central nervous system (CNS)-specific autoimmune lymphocytes" @default.
- W4313368802 doi "https://doi.org/10.4049/jimmunol.204.supp.142.33" @default.
- W4313368802 hasPublicationYear "2020" @default.
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