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Toll‐like receptors 2 and 3 enhance melanogenesis and melanosome transport in human melanocytes
Author(s) -
Koike Saaya,
Yamasaki Kenshi,
Yamauchi Takeshi,
Inoue Mai,
ShimadaOhmori Ryoko,
Tsuchiyama Kenichiro,
Aiba Setsuya
Publication year - 2018
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/pcmr.12703
Subject(s) - melanosome , tlr3 , tyrosinase , melanin , microbiology and biotechnology , innate immune system , tlr2 , epidermis (zoology) , biology , human skin , receptor , chemistry , toll like receptor , tlr4 , signal transduction , biochemistry , anatomy , genetics , enzyme
Summary Because little is known about how the innate immune response influences skin pigmentation, we examined whether Toll‐like receptor ( TLR ) agonists participate in melanogenesis and melanosome transportation. We observed that TLR 2/2 agonist HKLM and TLR 3 agonist Poly(I:C) increased the amount of extracellular melanin from primary human epidermal melanocytes. HKLM , but not Poly(I:C), increased the melanogenic genes such as tyrosinase and dopachrome tautomerase. Poly(I:C) increased the expression of Rab27A, a molecule that facilitates melanosome transport to perimembranous actin filament. UVB irradiation induced Rab27A and melanosome transportation in a similar manner of Poly(I:C). Si RNA for TLR 3 or Rab27A suppressed the perimembranous accumulation of Gp100‐positive vesicles in melanocytes and decreased melanin transfer to neighboring keratinocytes induced by both Poly(I:C) and UVB . These results suggest that the microenvironment in the epidermis and innate immune stimuli, such as microbiome and ultraviolet represented here by TLR 2 and TLR 3 agonists, could affect the melanogenesis in human melanocytes.