| First Author | Li L | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 5 | Pages | 2951-6 |
| PubMed ID | 18292517 | Mgi Jnum | J:131570 |
| Mgi Id | MGI:3773973 | Doi | 10.4049/jimmunol.180.5.2951 |
| Citation | Li L, et al. (2008) Splenic Stromal Microenvironment Negatively Regulates Virus-Activated Plasmacytoid Dendritic Cells through TGF-{beta}. J Immunol 180(5):2951-6 |
| abstractText | Plasmacytoid dendritic cells (pDCs) secrete large amounts of IFN-alpha upon exposure to virus, subsequently promoting and regulating innate and adaptive immune responses. However, little is known about the functional regulation of virus-activated pDCs after they exert functions in secondary lymph organs. Our previous studies show that splenic stromal microenvironment can down-regulate the T cell response by inducing generation of regulatory myeloid dendritic cells; therefore, we wondered whether the splenic stromal microenvironment can regulate the function of virus-activated pDCs. In this study, we provide evidences that the splenic stromal microenvironment can chemoattract vesicular stomatitis virus (VSV)-activated pDCs via stromal cell-derived dactor 1 (SDF-1), inhibit the secretion of IFN-alpha, IL-12, TNF-alpha, and expression of I-A(b), CD86, CD80, and CD40 by VSV-activated pDCs, and subsequently inhibit VSV-infected pDCs to activate NK cell IFN-gamma production and cytotoxicity. Stroma-derived TGF-beta participates in the negative regulation of VSV-activated pDCs. Therefore, we demonstrate that splenic stromal microenvironment negatively regulates the virus-activated pDCs through TGF-beta, outlining an additional mechanistic explanation for maintenance of immune homeostasis. |
