Role of CD7 in Skin Inflammation and Psoriasis

This study has been completed.
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00162825
First received: September 12, 2005
Last updated: July 9, 2008
Last verified: June 2003
  Purpose

Role of CD7 in skin inflammation and psoriasis


Condition
Psoriasis
Inflammation

Study Type: Observational

Resource links provided by NLM:


Further study details as provided by National Taiwan University Hospital:

Estimated Enrollment: 30
Study Start Date: January 2004
Study Completion Date: December 2006
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.

  Eligibility

Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

clinical diagnosis of psoriasis

Exclusion Criteria:

-

  Contacts and Locations
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Please refer to this study by its ClinicalTrials.gov identifier: NCT00162825

Locations
Taiwan
National Taiwan University Hospital
Taipei, Taiwan, 100
Sponsors and Collaborators
National Taiwan University Hospital
Investigators
Principal Investigator: whu-Liang Hwu, MD, PhD National Taiwan University Hospital
  More Information

No publications provided

ClinicalTrials.gov Identifier: NCT00162825     History of Changes
Other Study ID Numbers: 9261700717
Study First Received: September 12, 2005
Last Updated: July 9, 2008
Health Authority: Taiwan: Department of Health

Keywords provided by National Taiwan University Hospital:
Psoriasis, T cell, inflammation, CD7, cytokine

Additional relevant MeSH terms:
Inflammation
Psoriasis
Pathologic Processes
Skin Diseases, Papulosquamous
Skin Diseases

ClinicalTrials.gov processed this record on September 18, 2014