Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 140, Issue 6, Pages 1143-+Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2019.11.013
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- ATIP-AVENIR grant
- ANR JCJC grant
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Vitiligo is an autoimmune disease that results from the loss of melanocytes, associated with skin infiltration of CD8(+) effector memory T cells with a Tc1 skewed immune response. NKG2D is an activating receptor found on immune cells, in particular natural killer and activated CD8(+) T cells, that are able to produce a high amount of IFN-gamma. Here we found that NKG2D expression was increased in vitiligo skin CD8(+) effector memory T cells and was promoted by IL-15. Phenotypic and functional analyses showed that NKG2D(+) CD8(+) skin effector memory T cells displayed an activated phenotype and produced elevated levels of both IFN-gamma and tumor necrosis factor-alpha. Additional experiments revealed that vitiligo skin dendritic cells expressed the NKG2D ligands MICA-MICB, and in vitro experiments showed that these ligands could be induced on dendritic cells by IFN-alpha. Cultures of IFN-alpha-estimulated dendritic cells with skin NKG2D(+) CD8(+) T cells potentiated the production of type 1 cytokines, which was next inhibited by blocking the NKG2D/MICA-MICB interaction. These data show that NKG2D is a potential marker of pathogenic skin CD8(+) effector memory T cells during vitiligo. Therefore, targeting NKG2D could be an attractive strategy in vitiligo, a disease for which there is a strong need of innovative treatments.
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