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CD3+CD56+ NK T cells are significantly decreased in the peripheral blood of patients with psoriasis.

Abstract：

:Psoriasis is a chronic, inflammatory, hyperproliferative skin disease, in which autoimmunity plays a great role. Natural killer T cells (NK T cells), are suggested to be involved in the pathogenesis of different autoimmune diseases. To examine the involvement of CD3+CD56+ NK T cells in the pathogenesis of psoriasis, we investigated the lymphocyte subpopulations obtained from blood samples of psoriatic patients before and after treatment, and of healthy controls, using two-colour flow cytometry. We found no significant differences between total T cells, total B cells, T helper cells, T cytotoxic cells and NK cells in patients with psoriasis before and after treatment and in controls. Increased percentage of memory T cells and decreased percentage of naive T cells was detected in psoriatic patients compared to controls, but these changes were not statistically significant. The CD3+CD56+ cells of psoriatic patients were significantly decreased relative to controls. The percentage of CD3+CD56+ cells increased after different antipsoriatic therapies, but remained significantly lower than those found in controls. CD3+CD56+ cells of healthy controls were capable of rapid activation, while in psoriatic patients activated NK T cells were almost absent. The decrease in the number of CD3+CD56+ cells may represent an intrinsic characteristic feature of patients with psoriasis, which is supported by the fact that after treatment NK T cells do not reach the values found in controls. In conclusion our results suggest that CD3+CD56+ NK T cells could be actively involved in the development of Th1 mediated autoimmune diseases.

journal_name

Clin Exp Immunol

journal_title

Clinical and experimental immunology

authors

Koreck A,Surányi A,Szöny BJ,Farkas A,Bata-Csörgö Z,Kemény L,Dobozy A

doi

10.1046/j.1365-2249.2002.01721.x

subject

Has Abstract

pub_date

2002-01-01 00:00:00

pages

176-82

issue

1

eissn

0009-9104

issn

1365-2249

pii

1721

journal_volume

127

pub_type

杂志文章

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