Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 132, Issue 1, Pages 135-143Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2011.259
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Funding
- NIH [NIH R01 AR052728, NIH R01 AI052453]
- VA Merit Award
- National Psoriasis Foundation
- Grants-in-Aid for Scientific Research [24591622, 23591637] Funding Source: KAKEN
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Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands, such as CpG or genomic DNA, they greatly increased production of type I IFNs. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of IFN-beta than normal skin lacking LL-37. The mechanism for induction of type I IFNs in keratinocytes was dependent on TLR9 expression but not on a DNA-LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis.
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