| First Author | Vigne S | Year | 2012 |
| Journal | Blood | Volume | 120 |
| Issue | 17 | Pages | 3478-87 |
| PubMed ID | 22968459 | Mgi Jnum | J:191418 |
| Mgi Id | MGI:5461742 | Doi | 10.1182/blood-2012-06-439026 |
| Citation | Vigne S, et al. (2012) IL-36 signaling amplifies Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells. Blood 120(17):3478-87 |
| abstractText | The interleukin-1 (IL-1) superfamily of cytokines comprises a set of pivotal mediators of inflammation. Among them, the action of IL-36 cytokines in immune responses has remained elusive. In a recent study, we demonstrated a direct effect of IL-36 on immune cells. Here we show that, among T cells, the IL-36 receptor is predominantly expressed on naive CD4(+) T cells and that IL-36 cytokines act directly on naive T cells by enhancing both cell proliferation and IL-2 secretion. IL-36beta acts in synergy with IL-12 to promote Th1 polarization and IL-36 signaling is also involved in mediating Th1 immune responses to Bacillus Calmette-Guerin infection in vivo. Our findings point toward a critical function of IL-36 in the priming of Th1 cell responses in vitro, and in adaptive immunity in a model of mycobacterial infection in vivo. |
