Despite major advances in immunotherapeutic approaches designed to bolster endogenous immune responses against tumors, metastatic melanoma remains associated with high mortality and rapid progression. Development of novel approaches toward enhancing endogenous immune responses against melanoma constitutes a critical step toward the management of disease. Of note, initiating immune responses against non-mutated melanocyte-specific protein antigens has shown efficacy in augmenting immunotherapies. Vitiligo is an autoimmune disease characterized by immune-mediated destruction of melanocytes, though the etiology of this disease remains poorly understood. Microbes have been recently found to have a profound effect on immune processes of the skin, including those that are associated with vitiligo progression. Identifying skin-resident microbes that initiate or exacerbate anti-melanocyte immunity, as well as the precise pathways that mediate these processes, may provide a novel framework for the development of immunotherapies to augment anti-tumor immune responses and efficacy of existing therapies. Thus, we have recruited a cohort of individuals with vitiligo and profiled their skin microbiomes at various body sites. We have isolated numerous vitiligo-associated bacteria and have adapted a mouse model of vitiligo in order to understand mechanisms of host-microbiome interaction in this setting. Interrogation of such a relationship between the microbiome and autoimmune destruction of melanocytes in vitiligo may lead to the identification of novel targets and pathways by which to augment melanoma immunotherapies.

Citation Format: Ivan Vujkovic-Cvijin, Jacquice Davis, Rasnik Singh, Kristina Lee, Zhiya Yu, Nicholas Restifo, Maria Wei, Yasmine Belkaid. Cutaneous microbiota in development of endogenous anti-melanocyte immunity [abstract]. In: Proceedings of the Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; 2016 Sept 25-28; New York, NY. Philadelphia (PA): AACR; Cancer Immunol Res 2016;4(11 Suppl):Abstract nr A078.