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Abstract
Psoriasis is a hyperproliverative skin disorder that is believed to be one of the Th1 mediated autoimmune diseases. The Th1 cytokines polarity (IL-2 and INFγ) contributes to the pathogenesis of this disease may be due to an inherited defects in the immuno- regulatory cells that control the balance between Th1 and Th2 cells as NKT cells.
NKT cells are considered as one of these immunoregulatory cells. They are subpopulations of T cells that express both NK cell receptors (CD16, CD56 and NK1.1) and T cell receptors (TCR-CD3, CD2 and sometimes CD4). Unconventionally they recognize glycolipid antigens in association with CD1d molecules (i.e non MHC restricted).
Naturally peripheral blood CD4+NKT cells release cytokines as IL-4 and IL-10 which inhibit the Th1 cells. Th1 cells are the main stimulator of the immune system; They stimulate both innate (NK cells and APCs) and adaptive (Tc, Th and B cells) immune response.
In psoriasis (a Th1 mediated autoimmune diseases); deficiency of peripheral blood NKT cells was documented. This may be the cause of the over activity of the Th1 cells that was demonstrated in psoriasis.