PD-L1 produced by HaCaT cells under polyinosinic-polycytidylic acid stimulation inhibits melanin production by B16F10 cells

Minhwa Park, So Youn Woo, Kyung Ah Cho, Min Sun Cho, Kyung Ho Lee

Research output: Contribution to journalArticlepeer-review

9 Scopus citations

Abstract

Skin forms a physical barrier that protects the body against outside agents. The deepest layer of the skin, the stratum basale, contains two cell types: agent-sensing keratinocytes, and melanin-producing melanocytes. Keratinocytes can sense both harmless commensal organisms and harmful pathogens via Toll-like receptors (TLRs), and keratinocytes subsequently drive immune responses. Activation of TLR3 is required for barrier repair because it stimulates essential genes, including tight junction genes, and inflammatory cytokines. Within the basal layer of the skin, resident melanocytes use their dendritic processes to connect with approximately 30–40 neighboring keratinocytes. Most studies have focused on the transfer of melanin-synthesizing melanosomes from melanocytes to keratinocytes, but the potential regulation of melanogenesis by soluble factor(s) produced by keratinocytes remains to be explored. Studying such regulation in vivo is challenging because of the keratinocyte:melanocyte ratio in the epidermis and the location of the cells within the skin. Therefore, in this study, we investigated whether keratinocytes affected melanocyte melanogenesis in vitro under normal or inflammatory conditions. We found that polyinosinic-polycytidylic acid [poly(I:C)] stimulation induced PD-L1 secretion from HaCaT cells and that poly(I:C)-induced PD-L1 inhibited melanin production by B16F10 cells. These data provide key evidence that keratinocytes can alter melanocyte melanogenesis via the production of soluble factors under inflammatory conditions.

Original languageEnglish
Article numbere0233448
JournalPLoS ONE
Volume15
Issue number5
DOIs
StatePublished - May 2020

Bibliographical note

Publisher Copyright:
© 2020 Park et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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