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PLoS One. 2018 Jun 21;13(6):e0199601. doi: 10.1371/journal.pone.0199601. eCollection 2018.

High level expression of A2ARs is required for the enhancing function, but not for the inhibiting function, of γδ T cells in the autoimmune responses of EAU.

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Doheny Eye Institute and Department of Ophthalmology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States of America.
Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville, Louisville, Kentucky, United States of America.
Department of Biomedical Research, National Jewish Health, Denver, CO, United States of America.


We previously reported that activated γδ T cells greatly enhance autoimmune responses, particularly the Th17 response. To determine the mechanisms involved, we made a series of comparisons between activated and non-activated γδ T cells. Our results showed that activated γδ T cells expressed greatly increased levels of A2A adenosine receptor (A2AR) and decreased amounts of CD73, as well as increased amounts of T cell activation markers such as CD69, CD44 and CD25. We show that A2AR is a major functional molecule in the enhancing activity of γδ T cells. A2AR-/- γδ T cells (isolated from A2AR-/- mouse), lost their Th17-enhancing activity as did A2AR+/+ γδ T cells (isolated from wt-B6 mouse) after treatment with an A2AR antagonist. Since γδ T cells possess either an enhancing or an inhibiting effect, we also tested whether A2AR expression on γδ T cells is essential to their inhibiting effect. Our results showed that the inhibiting effect of A2AR-/- γδ T cells was as potent as that of A2AR+/+ γδ T cells. In a previous report we showed that the expression of different levels of CD73 molecule allowed γδ T cells to adjust their suppressive activity; in the current study, we show that expression of increased amounts of A2AR allows γδ T cells to more effectively exert their enhancing function.

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