| First Author | Schenk U | Year | 2008 |
| Journal | Sci Signal | Volume | 1 |
| Issue | 39 | Pages | ra6 |
| PubMed ID | 18827222 | Mgi Jnum | J:259500 |
| Mgi Id | MGI:6141361 | Doi | 10.1126/scisignal.1160583 |
| Citation | Schenk U, et al. (2008) Purinergic control of T cell activation by ATP released through pannexin-1 hemichannels. Sci Signal 1(39):ra6 |
| abstractText | T cell receptor (TCR) stimulation results in the influx of Ca(2+), which is buffered by mitochondria and promotes adenosine triphosphate (ATP) synthesis. We found that ATP released from activated T cells through pannexin-1 hemichannels activated purinergic P2X receptors (P2XRs) to sustain mitogen-activated protein kinase (MAPK) signaling. P2XR antagonists, such as oxidized ATP (oATP), blunted MAPK activation in stimulated T cells, but did not affect the nuclear translocation of the transcription factor nuclear factor of activated T cells, thus promoting T cell anergy. In vivo administration of oATP blocked the onset of diabetes mediated by anti-islet TCR transgenic T cells and impaired the development of colitogenic T cells in inflammatory bowel disease. Thus, pharmacological inhibition of ATP release and signaling could be beneficial in treating T cell-mediated inflammatory diseases. |
