Format

Send to

Choose Destination
PLoS Biol. 2018 May 3;16(5):e2003648. doi: 10.1371/journal.pbio.2003648. eCollection 2018 May.

A direct link between MITF, innate immunity, and hair graying.

Author information

1
Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America.
2
Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
3
Department of Biochemistry and Molecular Biology, University of Maryland, School of Medicine, Baltimore, Maryland, United States of America.
4
Computational and Statistical Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
5
Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
6
Research & Development Service, VA Maryland Health Care System, Baltimore, Maryland, United States of America.

Abstract

Melanocyte stem cells (McSCs) and mouse models of hair graying serve as useful systems to uncover mechanisms involved in stem cell self-renewal and the maintenance of regenerating tissues. Interested in assessing genetic variants that influence McSC maintenance, we found previously that heterozygosity for the melanogenesis associated transcription factor, Mitf, exacerbates McSC differentiation and hair graying in mice that are predisposed for this phenotype. Based on transcriptome and molecular analyses of Mitfmi-vga9/+ mice, we report a novel role for MITF in the regulation of systemic innate immune gene expression. We also demonstrate that the viral mimic poly(I:C) is sufficient to expose genetic susceptibility to hair graying. These observations point to a critical suppressor of innate immunity, the consequences of innate immune dysregulation on pigmentation, both of which may have implications in the autoimmune, depigmenting disease, vitiligo.

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center