2009 Fiscal Year Final Research Report
The roles of chemical mediators in the pathogenesis of psoriasis vulgaris and their therapeutical application
| Project/Area Number |
18591259
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Teikyo University |
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Principal Investigator |
KANDA Naoko Teikyo University, 医学部, 准教授 (50260493)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Shinichi 帝京大学, 医学部, 教授 (90114719)
ONISHI Takamitsu 帝京大学, 医学部, 准教授 (80233211)
TADA Yayoi 東京大学, 医学部附属病院, 講師 (00334409)
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| Project Period (FY) |
2006 – 2009
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| Keywords | 尋常性乾癬 / ケミカルメディエーター / ケラチノサイト |
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| Research Abstract |
Psoriasis vulgaris is an autoimmune inflammatory dermatosis. Chemical mediators may be involved in the pathogenesis of this disease. Prolactin acts on keratinocytes and induces their production of CXCL9/10/11 or CCL20 chemoattracting Th1/Tc1 cells or Th17 cells, respectively. Leukotriene B_4 acts on keratinocytes and induces their production of CCL27 chemoattracting skin-homing memory T cells. These mediators may induce the infiltration of T cells into psoriatic skin lesions via these chemokines. Leptin induces the production of antimicrobial peptide human β-defensin-2, and histamine induces human β-defensin-2 and human β-defensin-3 production in keratinocytes. These mediators may enhance the proliferation of keratinocytes, angiogenesis, and infiltration of Th17 cells in psoriatic skin lesions in addition to the enhancement of cutaneous antimicrobial activities.
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Research Products
(18 results)
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[Journal Article] Prolactin enhances basal and IL-17-induced CCL20 production by human keratinocytes.2009
Author(s)
Kanda, N., Shibata, S., Tada, Y., Nashiro, K., Tamaki, K., Watanabe, S.
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Journal Title
Eur J Immunol 39
Pages: 996-1006
Peer Reviewed
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