| First Author | Amir M | Year | 2020 |
| Journal | Biochem Biophys Res Commun | Volume | 527 |
| Issue | 4 | Pages | 1000-1007 |
| PubMed ID | 32439175 | Mgi Jnum | J:312115 |
| Mgi Id | MGI:6713329 | Doi | 10.1016/j.bbrc.2020.05.012 |
| Citation | Amir M, et al. (2020) Pharmacological modulation and genetic deletion of REV-ERBalpha and REV-ERBbeta regulates dendritic cell development. Biochem Biophys Res Commun 527(4):1000-1007 |
| abstractText | The nuclear receptors REV-ERBalpha and REV-ERBbeta have been demonstrated to play key roles in the regulation of numerous physiological functions, such as metabolism and the circadian rhythm. Recent studies have established the REV-ERBs' roles in immunity, including macrophage and T cell responses. In contrast, their roles in dendritic cells have not been well defined. Dendritic cells are potent antigen presenting cells, connecting microbial sensing and innate immunity to adaptive immune responses. We demonstrate that both REV-ERBalpha and REV-ERBbeta expression is upregulated during the course of bone marrow derived dendritic cell (BMDC) differentiation. BMDCs from REV-ERBalpha and REV-ERBbeta deficient mice showed enhanced expression of maturation markers like CD86, MHCII, and proinflammatory cytokines. Conversely, treatment of BMDCs with a REV-ERB-specific agonist, SR9009, inhibited the expression of maturation markers and proinflammatory cytokines. Our study suggests the REV-ERBs act as negative regulators of dendritic cell development and activation. These results indicate that pharmacological modulation of REV-ERB activity could be an attractive strategy to modulate DC activation status and for DC-based therapies. |
