| First Author | Liang D | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 6 | Pages | e0199601 |
| PubMed ID | 29928041 | Mgi Jnum | J:263744 |
| Mgi Id | MGI:6187848 | Doi | 10.1371/journal.pone.0199601 |
| Citation | Liang D, et al. (2018) High level expression of A2ARs is required for the enhancing function, but not for the inhibiting function, of gammadelta T cells in the autoimmune responses of EAU. PLoS One 13(6):e0199601 |
| abstractText | We previously reported that activated gammadelta 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 gammadelta T cells. Our results showed that activated gammadelta 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 gammadelta T cells. A2AR-/- gammadelta T cells (isolated from A2AR-/- mouse), lost their Th17-enhancing activity as did A2AR+/+ gammadelta T cells (isolated from wt-B6 mouse) after treatment with an A2AR antagonist. Since gammadelta T cells possess either an enhancing or an inhibiting effect, we also tested whether A2AR expression on gammadelta T cells is essential to their inhibiting effect. Our results showed that the inhibiting effect of A2AR-/- gammadelta T cells was as potent as that of A2AR+/+ gammadelta T cells. In a previous report we showed that the expression of different levels of CD73 molecule allowed gammadelta T cells to adjust their suppressive activity; in the current study, we show that expression of increased amounts of A2AR allows gammadelta T cells to more effectively exert their enhancing function. |
