Retinoid-X-Receptors (α/β) in Melanocytes Modulate Innate Immune Responses and Differentially Regulate Cell Survival following UV Irradiation
Figure 6
Mechanistic representation of post-UVR defects in Rxrα/βmel−/− mice compared to control mice.
In Rxrα/βL2/L2 control mice post-UVR, melanocytes recruit immune cells via secretion of chemoattractive and repulsive ligands (A). The recruited immune cells secrete IFN-y, which promotes survival of melanocytes/fibroblasts and stimulates additional chemokine secretion from melanocytes via a feedback loop (B). In Rxrα/βmel−/− mice, there is less secretion of chemoattractive and more secretion of chemorepulsive ligands from the melanocytes (C). As a result, fewer immune cells are recruited as a result of shift in the chemoattractive/repulsive ligands, resulting in reduced available IFN-y (D), negatively influencing fibroblast survival (E). (F) As RXRs α and β are ablated specifically in melanocytes, an endogenous shift in pro- and anti- apoptotic signals results in enhanced survival of melanocytes in Rxrα/βmel−/− mice relative to controls.