IL-35: a potential target for the treatment of atherosclerosis.

Ying Huang, Ying-zhong Lin, Ying Shi, Qingwei Ji
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引用次数: 17

Abstract

The imbalance of anti- inflammatory/pro-inflammatory cytokines plays an important role in the process of atherosclerosis. IL-35 is an anti-inflammatory cytokine comprising the p35 subunit of IL-12 and the subunit Epstein-Barr virus (EBV) -induced gene 3(EBI3). Accumulating evidence showed that IL-35 up-regulates the expression of anti-inflammatory cytokines, induces the generation of CD4 + regulatory T cells, inhibits CD4 + effector T cells response and other target cells activity, and reduces the progression of inflammatory and autoimmune diseases. In addition, it has been found that Ebi3 and p35 strongly coexpressed in human advanced lesions. Therefore, we hypothesize that IL-35 may become a novel target for the treatment of atherosclerosis. Further studies are required to investigate the precise effect and the signaling pathway of IL-35 in atherosclerosis process.
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IL-35:治疗动脉粥样硬化的潜在靶点
抗炎/促炎细胞因子失衡在动脉粥样硬化过程中起重要作用。IL-35是一种抗炎细胞因子,由IL-12的p35亚基和eb病毒诱导基因3(EBI3)亚基组成。越来越多的证据表明,IL-35上调抗炎细胞因子的表达,诱导CD4 +调节性T细胞的产生,抑制CD4 +效应T细胞反应和其他靶细胞活性,减缓炎症性和自身免疫性疾病的进展。此外,已经发现Ebi3和p35在人类晚期病变中强烈共表达。因此,我们假设IL-35可能成为动脉粥样硬化治疗的新靶点。IL-35在动脉粥样硬化过程中的确切作用及其信号通路有待进一步研究。
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