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首页> 外文期刊>Cytokine >Interferon (IFN)-inducible Absent in Melanoma 2 proteins in the negative regulation of the type I IFN response: Implications for lupus nephritis
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Interferon (IFN)-inducible Absent in Melanoma 2 proteins in the negative regulation of the type I IFN response: Implications for lupus nephritis

机译：干扰素（IFN） - 在黑色素瘤2中缺席的遗传学蛋白在I IFN响应类型中的负调节中：对狼疮性肾炎的影响

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摘要

Systemic lupus erythematosus (SLE) is a complex autoimmune disease that exhibits a strong female bias (femaleto-male ratio 9:1) in patients. Further, 40-60% SLE patients develop lupus nephritis (LN), which significantly increases the mortality rates. The failure of current therapies to adequately treat LN in patients reflects an incomplete understanding of the disease pathogenesis. Notably, a chronic increase in serum interferon-alpha (IFN-alpha) activity is a heritable risk factor to develop SLE. Accordingly, blood cells from most SLE patients with an active disease exhibit an increase in the expression of the type I IFN (IFN-alpha/beta)-stimulated genes (ISGs, also referred to as "IFN-signature"), a type I IFN response. Further, LN patients during renal flares also exhibit an "IFN-signature" in renal biopsies. Therefore, an improved understanding of the regulation of type I IFNs expression is needed. Basal levels of the IFN-beta through "priming" of IFN-alpha producing cells augment the expression of the IFN-a genes. Of interest, recent studies have indicated a role for the type I IFN-inducible Absent in Melanoma 2 proteins (the murine Aim2 and human AIM2) in the negative regulation of the type I IFN response through inflammasomedependent and independent mechanisms. Further, an increase in the expression of Aim2 and AIM2 proteins in kidney and renal macrophages associated with the development of nephritis. Therefore, we discuss the role of Aim2/AIM2 proteins in the regulation of type I IFNs and LN. An improved understanding of the mechanisms by which the Absent in Melanoma 2 proteins suppress the type I IFN response and modulate nephritis is key to identify novel therapeutic targets to treat a group of LN patients.
机译：Systemic Lupus红斑（SLE）是一种复杂的自身免疫疾病，患者表现出强烈的女性偏见（Femaleto-Maligal比例9：1）。此外，40-60％的SLE患者开发狼疮肾炎（LN），显着提高了死亡率。当前疗法在患者中充分治疗LN的失败反映了对疾病发病机制的不完全理解。值得注意的是，血清干扰素-α-α（IFN-α）活性的慢性增加是开发SLE的遗传危险因素。因此，来自大多数SLE有源疾病的血细胞表现出I IFN（IFN-α/β） - 刺激基因（ISGS，也称为“IFN-签名”）的表达增加，其类型IFN响应。此外，肾脏耀斑期间的LN患者还表现出肾活组织检查中的“IFN-签名”。因此，需要改进对I型IFNS表达的调节的理解。 IFN-β基础水平通过IFN-α产生细胞的“灌注”增加IFN-A基因的表达。感兴趣的是，最近的研究表明，在黑色素瘤2蛋白（鼠Aim2和人Aim2）中缺席的I IFN诱导的作用是通过炎症彼然相关的IFN响应的负调节和独立的机制。此外，与肾炎的发育相关的肾脏和肾巨噬细胞中AIM2和AIM2蛋白表达的增加。因此，我们讨论AIM2 / AIM2蛋白在I型IFNS和LN调节中的作用。改善了对黑色素瘤2蛋白中不存在的机制的理解抑制I IFN响应和调节肾炎是关键，以鉴定新的治疗靶标以治疗一组LN患者。

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