IL-4 Inhibits the Melanogenesis of Normal Human Melanocytes through the JAK2–STAT6 Signaling Pathway View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-02

AUTHORS

Hyun Choi, Hyunjung Choi, Jiyeon Han, Sun Hee Jin, Ju-Yearl Park, Dong Wook Shin, Tae Ryong Lee, Kwangmi Kim, Ai-Young Lee, Minsoo Noh

ABSTRACT

Skin diseases can be characterized by their predominant CD4-positive T-helper (Th) cell profiles. Chronic dermatological conditions often give rise to abnormal skin pigmentation. To understand the role of Th cells in pigmentation, the effects of the major Th cell cytokines, IFNγ, IL-4, and IL-17A, on melanogenesis were evaluated using cultured normal human melanocytes (NHMs) instead of relying on transformed melanoma cell lines. IL-4 directly inhibited melanogenesis in NHMs and downregulated both transcription and translation of melanogenesis-associated genes, such as microphthalmia-associated transcription factor (MITF) and dopachrome tautomerase. Despite the lack of a direct inhibition of melanin pigment synthesis, IFNγ and IL-17A increased the synthesis of an antimelanogenic cytokine IL-6 in NHMs. IFNγ activated signal transducers and activators of transcription 1 (STAT1) and STAT3 phosphorylation in NHMs, and IL-4 increased the STAT3 and STAT6 phosphorylation. The differential phosphorylation profile of STAT proteins between IFNγ and IL-4 may explain the difference in their effect on melanogenesis in NHMs. The IL-4-induced downregulation of melanogenesis was inhibited by treating NHMs with a JAK2 inhibitor AG490 or STAT6 siRNA. In conclusion, the involvement of the IL-4-induced JAK2-STAT6 signaling and the IFNγ- or IL-17A-dependent antimelanogenic IL-6 production should be considered as one of the mechanisms explaining the association with hypopigmention in skin diseases. More... »

PAGES

528-536

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/jid.2012.331

DOI

http://dx.doi.org/10.1038/jid.2012.331

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037539947

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22992805


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