Literature DB >> 20224694

Overexpression of CXCL16 in lesional psoriatic skin.

Shin-Taek Oh, Anja Schramme, Wolfgang Tilgen, Paul Gutwein, Jörg Reichrath.   

Abstract

BACKGROUND: Psoriasis is characterized as an autoimmune disease resulting in an exaggerated innate immune response. The CXC-chemokine ligand 16 (CXCL16) is described to function as an adhesion molecule, a scavenger receptor or as a soluble molecule it acts as a chemoattractant. CXCL16 has been reported to be expressed in a variety of inflammatory diseases. However, no information has been reported in the literature about the expression of CXCL16 in psoriatic skin.
PURPOSE: The present study was designed to analyze the expression and localization of CXCL16 in human psoriatic skin tissues.
RESULTS: In normal skin, cytpoplasmic expression of CXCL16 was increased in keratinocytes of upper epidermal cell layers as compared to the lower epidermal cell layers. In lesional psoriatic skin, CXCL16 immunoreactivity was increased in the cytoplasm of keratinocytes of lower epidermal layer kerartinocytes as compared to the normal epidermis. Cytoplasmic CXCL16 expression was increased in the capillary endothelial cells of psoriatic dermis as compared to capillary endothelial cells of the normal dermis. Notably, almost all inflammatory cells in the dermis were negative for CXCL16.
MATERIALS AND METHODS: Ten paraffinized specimens of human lesional psoriatic skin and five paraffinized specimens of normal skin were studied using an immunohistochemical streptavidinperoxidase technique.
CONCLUSION: We here report for the first time alterations in the immunohistochemical staining pattern of CXCL16 in lesional psoriatic skin compared to the normal skin. These results suggest that CXCL16 may play a role in the pathogenesis of psoriasis.

Entities:  

Keywords:  CXCL16; immunohistochemistry; psoriasis

Year:  2009        PMID: 20224694      PMCID: PMC2835901          DOI: 10.4161/derm.1.2.7750

Source DB:  PubMed          Journal:  Dermatoendocrinol        ISSN: 1938-1972


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