The research for immunological alteration in the pathogenesis of chronic inflammatory skin diseases including psoriasis, atopic dermatitis, SLE.
Not Applicable
Recruiting
- Conditions
- chronic inflammatory skin diseases including psoriasis, atopic dermatitis, SLE
- Registration Number
- JPRN-UMIN000019215
- Lead Sponsor
- Department of Dermatology, Kochi Medical School, Kochi University
- Brief Summary
TNF inhibitors directly target Th17 cells via attenuation of autonomous TNF/TNFR2 signalling in psoriasis. In vitro Th17-polarized cells from PBMC produced TNF-a in FACS analysis. In addition, TH17-polarized cells exhibited inceased expression of TNFR2. FACS and ELISA confirmed the reduction of IL-17A proteins levels by THF inhibitor. The treatment with anti-TNFR2 significantly down-regulated the production of IL-17A from Th17 cells from psoriasis patients as well as treatment with TNF inhibitor.
- Detailed Description
Not available
Recruitment & Eligibility
- Status
- Recruiting
- Sex
- All
- Target Recruitment
- 100
Inclusion Criteria
Not provided
Exclusion Criteria
Patients with other inflammatory skin diseases
Study & Design
- Study Type
- Observational
- Study Design
- Not specified
- Primary Outcome Measures
Name Time Method TNF blocker inhibitors down-regulate at least two distinct pathways to attenuate IL-17 signalling in psoriasis: a direct effect on Th17 cells and an indirect effect via other types of cells, such as TipDCs.
- Secondary Outcome Measures
Name Time Method Anti-TNFa antibody didn't affect Th1 pathway.