IL-7 secreted by keratinocytes induces melanogenesis via c-kit/MAPK signaling pathway in Melan-a melanocytes.

Abnormal melanin synthesis within melanocytes can result in pigmentary skin disorders. Although pigmentation alterations associated with inflammation are frequently observed, the precise reason for this clinical observation is still unknown. More specifically, although many cytokines are known to be critical for inflammatory skin processes, it is unclear how they affect epidermal melanocyte function. Here, we wanted to see how IL-7, a type I cytokine, affects melanocytes because cytokine is known to be associated with various skin diseases. To this end, Melan-a melanocytes were tested for expression of the IL-7 receptor α (IL-7Rα) and common gamma chain (γc) and their response to IL-7. IL-7 promotes melanogenesis in Melan-a melanocytes, resulting in increased intracellular tyrosinase activity and melanin content. It also upregulates the transcription of melanogenesis-related genes like MITF, tyrosinase, TRP1, and TRP2. IL-7 receptor α (IL-7Rα) and common gamma chain (γc) are interacted with c-kit in Melan-a melanocytes. IL-7 also activates the phosphorylated c-kit and its downstream target genes, such as ERK1/2, JNK, and p38 phosphorylation in Melan-a melanocytes. Furthermore, inhibition of c-kit by ISCK03, c-kit inhibitor, significantly reversed c-kit phosphorylation and MITF expression. We also showed that IL-7 induces melanogenesis via the c-kit/MAPK signaling pathway based on the findings of this study. In conclusion, Melan-a melanocytes express IL-7 receptors on their surface, and IL-7 treatment on Melan-a cells leads to melanogenesis via the c-kit/MAPK signaling pathway. These results could lead to new treatments for pigmentation disorders and provide insight into the immunological processes surrounding melanocytes.