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Role of CD7 in Skin Inflammation and Psoriasis

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00162825
Recruitment Status : Completed
First Posted : September 13, 2005
Last Update Posted : July 11, 2008
Information provided by:
National Taiwan University Hospital

Brief Summary:
Role of CD7 in skin inflammation and psoriasis

Condition or disease
Psoriasis Inflammation

Detailed Description:

Psoriasis is a debilitating, chronic inflammatory skin disorder characterized by scaly skin patches caused by infiltration of inflammatory cells into the dermis and epidermis, with secondary epidermal cell (keratinocyte) hyperproliferation. Psoriasis is a complex disease and a combination of genetic and environmental factors are likely to be causative. T-cell-mediated immune process, including cytokines (eg. IFN-γ) and chemokines, play an essential role in psoriasis. Susceptibility genes for psoriasis map to PSORS1 in the HLA region at chromosome 6p21, PSORS2 in the chromosome 17q24-q25, and others.

Recently our colleagues in the Academia Sinica and we performed a genome-wide linkage analysis with polymorphic microsatellites in one five-generation affected psoriasis kindred, and the result revealed a close linkage at D17S928, close to CD7. CD7+ T cells produce IFN-γ when activated, and have been located in skin inflammatory lesions. Therefore, in this study we first want to examine the role of CD7 in skin inflammations conditions. CD7+ cells will be stimulated by a variety of methods, and will be used to treat keratinocyte cultures or be injected intradermally to mice. We will watch for skin inflammation and possible proliferation and changes in keratinocytes. Possible changes in CD7 function in patients with psoriasis will be explored, for example, polymorphisms of the CD7 gene may predispose skin inflammation and abnormal interaction with the keratinocytes. CD7- T cells, which could be derived from CD7+ cells and are enriched in skin inflammation lesions, secrete the Th2 cytokine IL-5. We are also interested in the mechanism and the consequences of this CD7 shift. We hope this study will be helpful in the understanding and management of skin inflammation conditions, including psoriasis.

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Study Type : Observational
Estimated Enrollment : 30 participants
Study Start Date : January 2004
Actual Study Completion Date : December 2006

Resource links provided by the National Library of Medicine

MedlinePlus related topics: Psoriasis

Information from the National Library of Medicine

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Ages Eligible for Study:   Child, Adult, Older Adult
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

clinical diagnosis of psoriasis

Exclusion Criteria:


Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT00162825

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National Taiwan University Hospital
Taipei, Taiwan, 100
Sponsors and Collaborators
National Taiwan University Hospital
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Principal Investigator: whu-Liang Hwu, MD, PhD National Taiwan University Hospital
Layout table for additonal information Identifier: NCT00162825    
Other Study ID Numbers: 9261700717
First Posted: September 13, 2005    Key Record Dates
Last Update Posted: July 11, 2008
Last Verified: June 2003
Keywords provided by National Taiwan University Hospital:
Psoriasis, T cell, inflammation, CD7, cytokine
Additional relevant MeSH terms:
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Pathologic Processes
Skin Diseases, Papulosquamous
Skin Diseases