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Elevated Interleukin-36? And CD4+IL-36?+T Cells Are Involved in the Pathogenesis of Graves' Disease.

ABSTRACT: Background: IL-36? is involved in the pathogenesis of a variety of autoimmune diseases, but the relationship between IL-36? and Graves' disease (GD) has rarely investigated. In the present study, we aimed to explore the expression of IL-36? and elucidate the potential role of IL-36? in GD. Methods: The expression of IL-36? mRNA in peripheral blood mononuclear cells (PBMCs) from 32 newly diagnosed GD patients, 15 refractory GD patients and 30 normal controls (NC) was examined using quantitative real-time polymerase chain reaction (qRT-PCR). The level of IL-36? in serum from 46 newly diagnosed GD patients, 10 refractory GD patients and 24 NC was measured using enzyme linked immunosorbent assay (ELISA). The percentage of CD4+IL-36?+T cells was detected by flow cytometry. PBMCs from newly diagnosed GD patients and NC group were cultured in the presence or absence of recombinant human IL-36?, and the expression levels of IFN-?, TNF-?, IL-6, and IL-17A in culture supernatant were detected by cytokine array. Results: The expression of IL-36? mRNA in newly diagnosed GD patients was significantly higher than that in NC group (P = 0.019). IL-36? mRNA expression was positively associated with thyrotropin receptor antibody (TRAb) (P = 0.004, r = 0.498) in newly diagnosed GD patients. The level of IL-36? in serum from newly diagnosed GD patients was significantly higher than that in refractory GD patients and NC group (P = 0.01; P = 0.007). The percentage of CD4+IL-36?+T cells in newly diagnosed GD patients was significantly higher than that in NC group (P = 0.030). In GD group, recombinant human IL-36? stimulation resulted in the increase of INF-?, TNF-?, IL-6 and IL-17A (P = 0.015; P = 0.016; P = 0.039; P = 0.017). Conclusion: IL-36? and CD4+IL-36?+T cells may be involved in the pathogenesis of GD by promoting the production of Th1, Th2, and Th17 cytokines.

SUBMITTER: Yao QM

PROVIDER: S-EPMC6190875 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Elevated Interleukin-36α And CD4+IL-36α+T Cells Are Involved in the Pathogenesis of Graves' Disease.

Yao Qiu-Ming QM Li Ling L Song Zhen-Yu ZY Wang Bin B Qin Qiu Q An Xiao-Fei XF Zhang Jin-An JA

Frontiers in endocrinology 20181009

Background: IL-36α is involved in the pathogenesis of a variety of autoimmune diseases, but the relationship between IL-36α and Graves' disease (GD) has rarely investigated. In the present study, we aimed to explore the expression of IL-36α and elucidate the potential role of IL-36α in GD. Methods: The expression of IL-36α mRNA in peripheral blood mononuclear cells (PBMCs) from 32 newly diagnosed GD patients, 15 refractory GD patients and 30 normal controls (NC) was examined using ...[more]

PMID: 30356900

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Project description:In inflammatory skin conditions, such as psoriasis, vascular enlargement is associated with endothelial cell proliferation, release of cytokines and adhesion molecule expression. Interleukin (IL)-17A is a pro-inflammatory cytokine mainly secreted by T helper-17 cells that is critically involved in psoriasis pathogenesis. IL-36α, IL-36β and IL-36γ are also inflammatory cytokines up-regulated in psoriasis and induced by various stimuli, including IL-17A. In this study, we found that human keratinocytes are the main source of IL-36, in particular of IL-36γ. This cytokine was strongly induced by IL-17A and, together with IL-17A, efficiently activated human dermal microvascular endothelial cells (HDMECs), which expressed both IL-17 and IL-36 receptors. Both IL-36γ and IL-17A induced cell proliferation through specific molecular cascades involving ERK1/2 only or ERK1/2, STAT3 and NF-κB, respectively. We highlighted the intense IL-17A- and IL-36γ -dependent interplay between keratinocytes and HDMECs, likely active in the psoriatic lesions and leading to the establishment of a cytokine network responsible for the development and maintenance of the inflamed state. IL-17A or IL-36γ showed in HDMECs a synergic activity with TNF-α by potently inducing inflammatory cytokine/chemokine release and ICAM-1 expression. We also investigated the involvement of IL-36γ and VEGF-A, substantially reduced in lesional skin of psoriatic patients pharmacologically treated with the anti-IL-17A antibody Secukinumab. Importantly, keratinocyte-derived IL-36γ represented an additional pro-angiogenic mediator of IL-17A. We observed that keratinocyte-derived VEGF-A influenced proliferation but did not act on expression of adhesion molecules in HDMECs. On the other hand, inhibition of IL-36γ released by IL-17A-treated keratinocytes impaired either proliferation or ICAM-1 expression both in HDMECs and in an in vivo murine model of psoriasis. Taken together, our data demonstrated that IL-17A and IL-36γ are highly involved in endothelial cells/keratinocytes crosstalk in inflammatory skin conditions.

Dataset Information

Elevated Interleukin-36? And CD4+IL-36?+T Cells Are Involved in the Pathogenesis of Graves' Disease.

Publications

Elevated Interleukin-36α And CD4<sup>+</sup>IL-36α<sup>+</sup>T Cells Are Involved in the Pathogenesis of Graves' Disease.

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