| First Author | Li HS | Year | 2011 |
| Journal | Blood | Volume | 118 |
| Issue | 14 | Pages | 3879-89 |
| PubMed ID | 21828128 | Mgi Jnum | J:178408 |
| Mgi Id | MGI:5298307 | Doi | 10.1182/blood-2011-04-349761 |
| Citation | Li HS, et al. (2011) Cell-intrinsic role for IFN-alpha-STAT1 signals in regulating murine Peyer patch plasmacytoid dendritic cells and conditioning an inflammatory response. Blood 118(14):3879-89 |
| abstractText | Plasmacytoid dendritic cells (pDCs) reside in bone marrrow and lymphoid organs in homeostatic conditions and typically secrete abundant quantities of type I interferons (IFNs) on Toll-like receptor triggering. Recently, a pDC population was identified within Peyer patches (PPs) of the gut that is distinguished by its lack of IFN production; however, the relationship of PP pDCs to pDCs in other organs has been unclear. We report that PP pDCs are derived from common DC progenitors and accumulate in response to Fms-like tyrosine kinase 3 ligand, yet appear divergent in transcription factor profile and surface marker phenotype, including reduced E2-2 and CCR9 expression. Type I IFN signaling via STAT1 has a cell-autonomous role in accrual of PP pDCs in vivo. Moreover, IFN-alpha enhances pDC generation from DC progenitors by a STAT1-dependent mechanism. pDCs that have been developed in the presence of IFN-alpha resemble PP pDCs, produce inflammatory cytokines, stimulate Th17 cell generation, and fail to secrete IFN-alpha on Toll-like receptor engagement. These results indicate that IFN-alpha influences the development and function of pDCs by inducing emergence of an inflammatory (Th17-inducing) antigen-presenting subset, and simultaneously regulating accumulation of pDCs in the intestinal microenvironment. |
