| First Author | Liang D | Year | 2018 |
| Journal | PLoS One | Volume | 13 |
| Issue | 5 | Pages | e0197189 |
| PubMed ID | 29771938 | Mgi Jnum | J:263535 |
| Mgi Id | MGI:6159520 | Doi | 10.1371/journal.pone.0197189 |
| Citation | Liang D, et al. (2018) Ability of gammadelta T cells to modulate the Foxp3 T cell response is dependent on adenosine. PLoS One 13(5):e0197189 |
| abstractText | Whether gammadelta T cells inhibit or enhance the Foxp3 T cell response depends upon their activation status. The critical enhancing effector in the supernatant is adenosine. Activated gammadelta T cells express adenosine receptors at high levels, which enables them to deprive Foxp3+ T cells of adenosine, and to inhibit their expansion. Meanwhile, cell-free supernatants of gammadelta T cell cultures enhance Foxp3 T cell expansion. Thus, inhibition and enhancement by gammadelta T cells of Foxp3 T cell response are a reflection of the balance between adenosine production and absorption by gammadelta T cells. Non-activated gammadelta T cells produce adenosine but bind little, and thus enhance the Foxp3 T cell response. Activated gammadelta T cells express high density of adenosine receptors and have a greatly increased ability to bind adenosine. Extracellular adenosine metabolism and expression of adenosine receptor A2ARs by gammadelta T cells played a major role in the outcome of gammadelta and Foxp3 T cell interactions. A better understanding of the functional conversion of gammadelta T cells could lead to gammadelta T cell-targeted immunotherapies for related diseases. |
