Inflammation Clinical Trial
Role of CD7 in skin inflammation and psoriasis
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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