| First Author | Conche C | Year | 2009 |
| Journal | Immunity | Volume | 30 |
| Issue | 1 | Pages | 33-43 |
| PubMed ID | 19144315 | Mgi Jnum | J:143721 |
| Mgi Id | MGI:3828870 | Doi | 10.1016/j.immuni.2008.10.020 |
| Citation | Conche C, et al. (2009) T cell adhesion primes antigen receptor-induced calcium responses through a transient rise in adenosine 3',5'-cyclic monophosphate. Immunity 30(1):33-43 |
| abstractText | It is well established that sustained increases in cyclic AMP (cAMP) such as those triggered by forskolin inhibit T cell activation. We describe here an unexpected phenomenon: in T cells, a transient cAMP increase triggered by the interaction with a dendritic cell strongly potentiates T cell receptor (TCR) signaling. We discovered this effect by examining the molecular basis of the adhesion-dependent sensitization of T cells. T cell adhesion caused extracellular-signal-regulated kinase (ERK) activation, which was necessary for the sensitization process. T cell sensitization could be mimicked in suspended cells by the uncaging of caged cAMP upon ultraviolet illumination. Calcium responses occurring in T cells upon interaction with dendritic cells were strongly inhibited when protein kinase A activation was blocked. Thus, whereas sustained cAMP increases are well known to inhibit TCR signaling, transient cAMP increases occurring physiologically upon formation of an immunological synapse facilitate antigen detection. |
