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home:diseases:psoriasis [04.08.2011] – paulalbert | home:diseases:psoriasis [08.30.2012] – paulalbert | ||
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====== Psoriasis ====== | ====== Psoriasis ====== | ||
- | J Clin Microbiol. 2006 Aug; | ||
- | Molecular analysis of fungal microbiota in samples from healthy human skin and psoriatic lesions. | ||
- | Paulino LC, Tseng CH, Strober BE, Blaser MJ. | ||
- | Department of Medicine, New York University School of Medicine, 550 First Ave., OBV-A 606, New York, NY 10016, USA. | ||
- | Psoriasis, a common cutaneous disease of unknown etiology, may be triggered by infections, including those due to fungi. Since the fungal community of human skin is poorly characterized, | ||
- | PMID: 16891514 | ||
- | Exp Dermatol. 2010 Aug; | + | ==== L-forms ==== |
- | Topical calcitriol protects from UV-induced genetic damage but suppresses cutaneous immunity in humans. | + | |
- | Damian DL, Kim YJ, Dixon KM, Halliday GM, Javeri A, Mason RS. | + | |
- | Dermatology, | + | |
- | Abstract | + | |
- | Calcitriol, the biologically active form of vitamin D, has been reported to cause both suppressive and protective immune effects in mice. Its immune effects in vivo in humans are unclear. We investigated the in vivo effects of topical calcitriol on minimal erythema dose and skin immune responses in healthy volunteers. We found that calcitriol did not protect from ultraviolet (UV)-induced erythema (sunburn) when applied either 24 h before or immediately after irradiation, | + | |
- | PMID: 19758324 | ||
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- | Narrow-band ultraviolet-B (NB-UVB) phototherapy is an effective treatment for psoriasis. The molecular mechanisms underlying its efficacy are incompletely understood. To identify NB-UVB-induced molecular pathways that may account for its anti-inflammatory efficacy, gene expression profiling was performed using epidermal RNA from lesional and nonlesional skin from patients with psoriasis undergoing NB-UVB therapy. Downregulation of Th17 signaling pathway was observed during NB-UVB therapy in psoriatic epidermis. Strong inhibition of the Th17 pathway by UVB was confirmed in an ex vivo organ culture system by demonstrating reduced signal transducer and activator of transcription 3 (STAT3) phosphorylation and -defensin-2 production. These results were further substantiated by demonstrating that NB-UVB inhibited the Th17-dependent psoriasis-like dermatitis in mice. Other pathways affected by NB-UVB therapy include the IFN signaling pathway, epidermal differentiation, | ||
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===== Evidence of infectious cause ===== | ===== Evidence of infectious cause ===== | ||
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microorganisms and psoriasis(({{pubmed> | microorganisms and psoriasis(({{pubmed> | ||
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