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KMID : 0984920150170020005
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Journal of Skin Barrier Research
2015 Volume.17 No. 2 p.5 ~ p.8
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Innate Immunity of Keratinocytes As a Pathogenesis of Psoriasis
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Shin Jung-Min
Choi Dae-Kyoung
Kim Sue-Jeong
Sohn Kyung-Cheol
Kim Chang-Deok
Lee Jeung-Hoon
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Abstract
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For skin to protect our body from the harmful attack of the environment, keratinocytes (KCs), the major cells of the epidermis, use a vareity of immune reactions which might result in chronic inflammation from their disturbed responses. Especially, nucleic acids (NA) derived from multiple microbes in constant contact with KCs could lead to inflammation through toll-like receptors (TLRs), types of pattern recognition receptors that recognize pathogen-associated molecular patterns present in microbes. Imiquimod, used to treat several skin diseases as a specific TLR7 ligand, stimulates NF-kB, IL-8 and TNF-a expression in KCs via TLR7. When KCs were stimulated with CpG ( TLR9 ligand), or poly(I:C) (TLR3 ligand), IL-17A expression was significantly increased, together with increase of other cytokines such as TNF-α and CCL20. IL-17A secreted from keratinocytes can stimulate CD4+ T cells, leading to strong induction of IL-22 production. As IL-22 is an important regulator of psoriatic inflammation, these data suggest that KCs can contribute to the pathogenesis of psoriasis by triggering the innate immune reaction through TLRs, and then affecting the activation of adaptive immune system involving CD4+ T cells. Finally we also found that cucurbitacin B has an inhibitory potential on imiquimod-induced inflammation of KCs, implicating that the modulation of inflammatory pathways in KCs could provide therapeutic potential for many inflammatory skin diseases.
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KEYWORD
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Keratinocytes, Innate immunity, Toll-like receptors, Psoriasis
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