| First Author | Nobs SP | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 10 | Pages | 3015-3035 |
| PubMed ID | 28798029 | Mgi Jnum | J:249867 |
| Mgi Id | MGI:5923305 | Doi | 10.1084/jem.20162069 |
| Citation | Nobs SP, et al. (2017) PPARgamma in dendritic cells and T cells drives pathogenic type-2 effector responses in lung inflammation. J Exp Med 214(10):3015-3035 |
| abstractText | Type-2 immune responses are well-established drivers of chronic inflammatory diseases, such as asthma, and represent a large burden on public health systems. The transcription factor PPARgamma is known to promote M2-macrophage and alveolar macrophage development. Here, we report that PPARgamma plays a key role in both T cells and dendritic cells (DCs) for development of type-2 immune responses. It is predominantly expressed in mouse Th2 cells in vitro and in vivo as well as human Th2 cells from allergic patients. Using conditional knockouts, we show that PPARgamma signaling in T cells, although largely dispensable for IL-4 induction, is critical for IL-33-driven Th2 effector function in type-2 allergic airway responses. Furthermore, we demonstrate that IL-4 and IL-33 promote up-regulation of PPARgamma in lung-resident CD11b(+) DCs, which enhances migration to draining lymph nodes and Th2 priming capacity. Thus, we uncover a surprising proinflammatory role for PPARgamma and establish it as a novel, important mediator of DC-T cell interactions in type-2 immunity. |
