Keywords
Toll-like receptors
immunity
erythroderma
How to Cite
Abstract
The article reviews current views on the role of Tоll-like receptors in the innate immune system, discusses their role in psoriasis. We also present our own data on the determination of Tоll-like receptors of 2 and 4 types in the blood of patients with various clinical forms of psoriasis in the advanced stage. In determining the leading criteria for the etiopathogenesis of psoriasis by establishing the role of Toll-like receptors (TLR) triggering exogenous psoriasis factors that can activate different types of immune cells, it was found that the expression level of TLR2 and TLR4 in different clinical forms of psoriasis in the advanced stage differed, namely: there was a tendency to increase the expression of TLR4 on lymphocytes (8±0.31 mfi) and almost did not differ from the control values (3.3±0.26 mfi) at lPsV (3.5±0.29 mfi). Statistically significant results were obtained to increase the expression of TLR4 in other clinical forms of psoriasis in the advanced stage: with PsP the level of TLR4 expression was increased 3.2 times, with PsG – 2.8 times, with PsE – 2.7 times, at dPsV – 2 times compared with the control. When determining the expression of TLR2 on lymphocytes, it was found that its level significantly exceeded similar indicators of the control group: with PsP and PsG – 2 times, with PsE – 1.6 times, with dPsV – 2 times, with PsF and lPsV – 1.5 times. The results obtained from the study can be explained by the fact that TLR2 and TLR4 are activated by pathogenic factors of microorganisms that grow on both affected and intact areas of the skin of patients with psoriasis in the advanced stage of the disease, their expression is increased by proinflammatory cytokines. A slight increase in TLR4 expression in lPsV and PsF may be associated with excessive stimulation of Toll receptors by exogenous ligands before or at the onset of the disease and the development of TLR refractory in the subsequent development
of disease and in some cases is a protective response to hyperergic inflammation.
Keywords: psoriasis, Toll-like receptors, immunity, erythroderma.
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