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.
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...
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Public Library of Science (PLoS)
2018-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0199601&type=printable |
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| author | Dongchun Liang Hui Shao Willi K Born Rebecca L O'Brien Henry J Kaplan Deming Sun |
| author_facet | Dongchun Liang Hui Shao Willi K Born Rebecca L O'Brien Henry J Kaplan Deming Sun |
| author_sort | Dongchun Liang |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T01:55:33Z |
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| id | doaj.art-0f138dd9efc742369bb0d95489fbbda9 |
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| issn | 1932-6203 |
| language | English |
| last_indexed | 2025-03-14T14:14:00Z |
| publishDate | 2018-01-01 |
| publisher | Public Library of Science (PLoS) |
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| spelling | doaj.art-0f138dd9efc742369bb0d95489fbbda92025-02-27T05:34:37ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01136e019960110.1371/journal.pone.0199601High 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.Dongchun LiangHui ShaoWilli K BornRebecca L O'BrienHenry J KaplanDeming SunWe 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.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0199601&type=printable |
| spellingShingle | Dongchun Liang Hui Shao Willi K Born Rebecca L O'Brien Henry J Kaplan Deming Sun 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. PLoS ONE |
| title | 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. |
| title_full | 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. |
| title_fullStr | 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. |
| title_full_unstemmed | 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. |
| title_short | 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. |
| title_sort | 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 |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0199601&type=printable |
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