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Expression of dipeptidyl‐peptidase IV (CD26) on CD8 + T cells is significantly decreased in patients with psoriasis vulgaris and atopic dermatitis
Author(s) -
Bock O.,
Kreiselmeyer I.,
Mrowietz U.
Publication year - 2001
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1034/j.1600-0625.2001.100604.x
Subject(s) - atopic dermatitis , psoriasis , scorad , medicine , cd8 , immunology , t cell , population , antigen , immune system , environmental health , dermatology life quality index
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‐to‐cell interaction and by the secretion of pro‐inflammatory mediators. CD26 is a lymphocyte membrane‐associated dipeptidyl peptidase IV (DPP IV), which is able to inactivate chemokines such as RANTES or eotaxin by cleaving dipeptides from the NH 2 −terminus of proteins. We investigated the expression of CD26 on CD4 + and CD8 + peripheral blood T cells in patients with psoriasis and atopic dermatitis. In addition PASI and SCORAD as a measure of disease 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 there is a significant decrease ( P <0.05) of CD26 expression on CD8 + T cells 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 disease severity as determined by PASI and SCORAD, respectively. Since CD26 can be regarded as an anti‐inflammatory principle the decreased expression in psoriasis and atopic dermatitis patients may lead to a dysbalance in favour of pro‐inflammatory mediators in both clinical conditions.