| First Author | Nasti TH | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 2 | Pages | 950-961 |
| PubMed ID | 28003381 | Mgi Jnum | J:253109 |
| Mgi Id | MGI:5925661 | Doi | 10.4049/jimmunol.1601455 |
| Citation | Nasti TH, et al. (2017) IL-23 Inhibits Melanoma Development by Augmenting DNA Repair and Modulating T Cell Subpopulations. J Immunol 198(2):950-961 |
| abstractText | In animal models, IL-12 and IL-23 participate in the development of malignant neoplasms of keratinocytes. However, the role of these cytokines in pigmented lesion development and their progression to melanoma has received little attention. IL-12p35, IL-23p19, and IL-12/IL-23p40 knockout mice on a C3H/HeN background, subjected to a melanomagenesis protocol, demonstrated profound differences in susceptibility to nevus initiation, transformation, tumorigenicity, and metastatic potential. IL-23 was found to be essential for melanocyte homeostasis, whereas IL-12 supported nevus development. A direct action of IL-23 on primary melanocytes, shown to be IL-23R+, demonstrated that DNA repair of damaged melanocytes requires IL-23. Furthermore, IL-23 modulated the cutaneous microenvironment by limiting regulatory T cells and IFN-gamma and inhibiting IL-10 production. Neutralizing Ab to IFN-gamma, but not IL-17, inhibited nevus development (p < 0.01). |
