1999 Fiscal Year Final Research Report Summary
MOLECULAR MECHANISMS AND CLINICAL APPLICATION OF ULTRAVIOLET A THERAPY
| Project/Area Number |
10670801
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | NAGOYA CITY UNIVERSITY |
|---|
Principal Investigator |
MORITA Akimichi NAGOYA CITY UNIVERSITY MEDICAL SCHOOL, DERMATOLOGY, ASSISTANT PROFESSOR, 医学部, 講師 (30264732)
|
|---|
| Project Period (FY) |
1998 – 1999
|
| Keywords | ULTRAVIOLET RADIATION / PHOTOTHERAPY / SKIN DISEASE / SCLEROSIS / APOPTOSIS / FAS / COLLAGEN / METALLOPROTEINASE |
|---|
| Research Abstract |
The purpose of this study was to investigate the underlying mechanisms and the clinical application of UVA1 phototherapy for skin diseases, e.g., atopic dermatitis, cutaneous T cell lymphoma and systemic sclerosis. UVA1 can penetrate through the epidermis to the deep dermis. No apoptosis was induced in keratinocytes and fibroblasts with 30-50 J/cmィイD12ィエD1 of UVA1 (430-400), which easily mediated T cell apoptosis. UVA1 induced FASL surface expression in keratinocytes if they were treated with metalloprotease inhibitor. Soluble FASL (sFASL) was also detected in the supernatant of UVA1-irradiated keratinocytes. The supernatant mediated apoptosis of FAS-expressing T cells with the treatment of the supernatant, which was partially inhibited with FASL antibody. The result suggested that sFASL from UVA1-irradiated keratinocytes mediated apoptosis of the infiltrating T cells in the lesion through paracrine mechanism. In fibroblasts, UVA1 upregulated metalloprotease (MMP)1, 3 but not TIMP-1, 3. It suggested that UVA1 might be effective for fibrous diseases, e.g., scleroderma. Based on the in vitro results, UVA1 therapy was attempted for the treatment of cutaneous malignant T cells and systemic sclerosis. The therapeutic effectiveness was found in both diseases.
|
Research Products
(15 results)
