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Abstract
Psoriasis is one of the immune-mediated inflammatory diseases (IMID); Both CD4⁺ T lymphocytes mainly Th1 cells and B lymphocytes contribute in the pathogenesis of IMIDs through the proinflammatory effect and production of antibodies, activation of T cells, cytokine synthesis respectively. Gamma delta (Þe) T cells are capable of producing large amounts of IL-17 upon IL-23 stimulation. The capacity of Þe T cells to produce IL-17 is acquired during thymic differentiation, independent of TCR signaling, a feature pointing to their innate nature. B and T lymphocyte attenuator (BTLA) is a coinhibitory molecule expressed on T and B lymphocytes as well as other immune cells, it is necessary to inhibit homeostatic expansion and activation of lymph node and skin resident Þe T cells. BTLA expression is regulated by RORÞt and IL-7. RORÞt is a key transcription factor driving the Th17 differentiation producing IL-17 which plays a major role in psoriasis pathogenesis. IL-7 plays a role in psoriasis pathogenesis and is also critical for the normal homeostasis, function, expansion, and survival of adult Þe Tcells. Aim of study: To add more insight to the role played by co-inhibitory molecule BTLA in psoriasis vulgaris patients, by studying the gene expression of BTLA, RORÞt and IL-7 in psoriasis patients. It also aimed to analyze their inter-relationship. This aims at establishing a basis for novel treatment strategies for psoriasis. Patients and methods: This case control study included 25 patients and 25 controls examined for gene expression of BTLA, RORÞt and IL-7