Activation of Toll-like Receptors 1, 2, 4, 5, and 7 on Human Melanocytes Modulate Pigmentation
Human melanocytes are not simply pigment-producing cells. It may be part of the inflammatory response, during which the pigmentary system may produce more melanin or suppress melanization. Toll-like receptors (TLRs) have been implicated in both innate host defense against pathogens and inflammatory...
Saved in:
Published in | Annals of dermatology Vol. 22; no. 4; pp. 486 - 489 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Korean Dermatological Association; The Korean Society for Investigative Dermatology
01.11.2010
대한피부과학회 |
Subjects | |
Online Access | Get full text |
ISSN | 1013-9087 2005-3894 2005-3894 |
DOI | 10.5021/ad.2010.22.4.486 |
Cover
Loading…
Summary: | Human melanocytes are not simply pigment-producing cells. It may be part of the inflammatory response, during which the pigmentary system may produce more melanin or suppress melanization. Toll-like receptors (TLRs) have been implicated in both innate host defense against pathogens and inflammatory response. Therefore, it may be possible that activation of TLRs in melanocytes may play a role in the modulation of melanogenesis. In this study, we investigated whether normal human melanocytes expressed TLRs and analyzed pigmentation changes upon TLR stimulation. The expression of TLR1~10 mRNA in cultured human melanocyte was analyzed using RT-PCR, Western blotting and immunocytochemistry. Human melanocytes constitutively express mRNA and protein for TLR2, 3, 4, 5, 7, 9 and 10. Stimulation of TLR1/2 and 4 with Pam3CSK4 and lipopolysaccharide induced pigmentation of melanocytes. Activation of TLR5 and 7 with flagellin and imiquimod treatments reduced pigmentation of melanocytes and zebrafish. In summary, the results provided evidence for TLRs expression in normal human melanocytes. It is speculated that a response of melanocyte to TLR ligands may play a role in the pigmentary change in the skin. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 G704-002233.2010.22.4.009 |
ISSN: | 1013-9087 2005-3894 2005-3894 |
DOI: | 10.5021/ad.2010.22.4.486 |