PSORIASIS - COMPARISON OF IMMUNOLOGICAL MARKERS IN PATIENTS WITH ACUTE AND REMISSION PHASE

Citation
O. Depita et al., PSORIASIS - COMPARISON OF IMMUNOLOGICAL MARKERS IN PATIENTS WITH ACUTE AND REMISSION PHASE, Journal of dermatological science, 13(2), 1996, pp. 118-124
Citations number
29
Categorie Soggetti
Dermatology & Venereal Diseases
ISSN journal
09231811
Volume
13
Issue
2
Year of publication
1996
Pages
118 - 124
Database
ISI
SICI code
0923-1811(1996)13:2<118:P-COIM>2.0.ZU;2-6
Abstract
The immune system involvement in psoriasis has been documented by the presence of activated T-cells both in peripheral blood and in psoriati c skin lesions and by the intervention of cytokines in the inflammator y process. On this basis, we have undertaken a study in order to exami ne, in addition to activation markers such as CD25 and CD54 (ICAM-1) o n peripheral blood mononuclear cells (PBMNCs) surface, serum levels of soluble interleukin (IL)-2 receptor (sIL-2R), soluble ICAM-1 (sICAM-1 ), soluble CD4 (sCD4), soluble CD8 (sCD8), beta 2-microglobulin and fi bronectin (FN) in psoriatic patients analyzed both in acute and remiss ion phase obtained by topical therapy alone. Our results show that PBM NCs expressing IL-2 receptor (CD25) were increased both in percentage and absolute number in respect to controls, and were not modified afte r remission. On the contrary, the significantly higher number of CD54( +) lymphocytes evaluated in acute psoriasis, showed a reduction during the remission phase, even if the values persisted higher than control s. Serum levels of sIL-2R, sICAM-1, sCD4, sCD8 and beta 2-microglobuli n were significantly higher than controls both in acute and remission phase; only FN levels were found to be lower, in patients evaluated bo th in acute psoriasis and after therapy, in respect to normal donors. On the whole, these results seem to indicate the persistence of both c ellular and soluble activation markers even in psoriasis remission pha se; in this light, we can suppose that topical therapy alone is not ab le to efficiently down-regulate activation mechanisms involved in the pathogenesis of the disease.