Abstract
Dermatitis herpetiformis (DH), bullous pemphigoid (BP), and pemphigus vulgaris (PV) are autoimmune bullous skin conditions with eosinophilic and neutrophilic infiltrations. While cytokines are crucial for the affinity and activation of different leukocyte cells in the inflammation and blister formation, there are no studies concerning a role of IL-36. The goal of the study was to analyze whether interleukin 36 is involved in pathogenesis of DH, BP, and PV. And the second aim of the study was the estimation of correlation between Il-36 and IL-17 and titers of specific antibodies in these diseases. Expression of IL-36 and IL-17 was detected in serum in all DH, BP, and PV samples. Serum levels of IL-36 and IL-17α were statistically higher in DH, BP, and PV groups as compared to the control group. IL-36α levels were statistically higher in DH patients, as compared to patients with PV and BP. Our results showed that IL-36 may be helpful in the diagnostic and monitoring of the activity of the disease. IL 36 may play a relevant role of enrolling eosinophils and neutrophils in DH, BP, and PV and finally provoke tissue injury.
Highlights
Interleukin 36 (IL-36) (α, β, γ) and IL-36Ra, called IL-36 cytokines, are recent members of the IL-1 family of cytokines [1] engaged in the evolution of diseases such as psoriasis [2, 3]
In Dermatitis herpetiformis (DH), the influx is consisted of neutrophils in the blister fluid, while in bullous pemphigoid (BP), bullae; the infiltrate is organized from mixed cells: neutrophils, eosinophils, lymphocytes, and histiocytes
Our findings showed that IL-36α is overexpressed in autoimmune blistering diseases, especially in DH and pemphigus vulgaris (PV) and BP too
Summary
Interleukin 36 (IL-36) (α, β, γ) and IL-36Ra, called IL-36 cytokines, are recent members of the IL-1 family of cytokines [1] engaged in the evolution of diseases such as psoriasis [2, 3]. IL-36 appears to exert a proinflammatory action by mediating the crosstalk among dendritic and another skin cells, the enrollment of inflammation cells, and the increase of γδ T cells [5]. Ciccia et al [6] confirmed that γδ T cells highly signify the IL-36R and generate elevated levels of IL-36 and IL-17. This is a proof of a proinflammatory role of IL-17+ IL-36+ γδ T lymphocytes in the immunological responses of the primary Sjogren’s syndrome.
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