Expression of dipeptidyl-peptidase IV (CD26) on CD8(+) T cells is significantly decreased in patients with psoriasis vulgaris and atopic dermatitis

Citation
O. Bock et al., Expression of dipeptidyl-peptidase IV (CD26) on CD8(+) T cells is significantly decreased in patients with psoriasis vulgaris and atopic dermatitis, EXP DERMATO, 10(6), 2001, pp. 414-419
Citations number
19
Categorie Soggetti
Dermatology
Journal title
EXPERIMENTAL DERMATOLOGY
ISSN journal
09066705 → ACNP
Volume
10
Issue
6
Year of publication
2001
Pages
414 - 419
Database
ISI
SICI code
0906-6705(200112)10:6<414:EODI(O>2.0.ZU;2-U
Abstract
T cells play a major role in inflammatory skin disorders such as psoriasis vulgaris and atopic dermatitis. They are both active on the level of cell-t o-cell interaction and by the secretion of pro-inflammatory mediators. CD26 is a lymphocyte membrane-associated dipeptidyl peptidase IV (DPP IV), whic h is able to inactivate chemokines such as RANTES or eotaxin by cleaving di peptides from the NH2-terminus of proteins. We investigated the expression of CD26 on CD4(+) and CD8(+) peripheral blood T cells in patients with psor iasis and atopic dermatitis. In addition PASI and SCORAD as a measure of di sease severity were determined in each patient at the time of blood drawing . Thirty patients with psoriasis, 15 with atopic dermatitis and 17 age- and sex-matched healthy persons were investigated by two-colour flow cytometry using epitope-specific monoclonal antibodies. Our results revealed, that t here is a significant decrease (P <0.05) of CD26 expression on CD8(+) T cel ls in both psoriasis (7.7%+/-3.3, mean and SD, n=30) and atopic dermatitis patients (7.9%+/-3.7, mean and SD, n=15) compared to the control population (11.58%+/-5.0, mean and SD, n=17). However, there was no correlation to di sease severity as determined by PASI and SCORAD, respectively. Since CD26 c an be regarded as an anti-inflammatory principle the decreased expression i n psoriasis and atopic dermatitis patients may lead to a dysbalance in favo ur of pro-inflammatory mediators in both clinical conditions.