AIMing 2 promote lupus by targeting helpers.
AIMing 2 promote lupus by targeting helpers.
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DOI：
10.1002/ctm2.844
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发表时间：
2022-05
影响因子：
10.6
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中科院分区：
文献类型：
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免疫系统在保护自身的同时，保护身体免受外来或危险入侵者的侵害。如果它将自我误认为非自我，那么它就会攻击人体自身的组织，导致自身免疫性疾病，如系统性红斑狼疮（SLE）。SLE是最常见的狼疮类型。许多器官，包括皮肤、关节、肺、肾和脑，都可能受到影响，并表现为广泛的炎症和组织损伤。针对自身核成分的广谱自身抗体的积累是SLE的标志。1滤泡辅助性T（TFH）细胞是CD 4 + T辅助性（TH）细胞的一个亚群，是生殖中心（GC）B细胞精确控制抗体产生所必需的。2，3众所周知，TFH细胞的过度扩张或失调是促进狼疮发病机制的自身反应性抗体的异常产生的根源。4因此，对TFH细胞分化和功能控制机制的更深入理解可能有助于开发治疗SLE的疗法。Wu等提出了一种新的机制，通过该机制，SLE患者的TFH反应可能失调。发现与健康对照相比，在狼疮患者的外周血和皮肤病变中的TFH样细胞（CD 4 + Bcl 6 + PD 1+）中，黑色素瘤2（人AIM 2和鼠AIM 2）中的Absent表达增加。AIM 2水平的升高归因于羟甲基转移酶10 - 11易位的募集增加。
The immune system defends the body against foreign or dangerous invaders while protecting the self. If it mistakes self for non-self, then it attacks the body’s own tissues, causing autoimmune disorders, such as systemic lupus erythematosus (SLE). SLE is the most common type of lupus. Many organs, including the skin, joint, lung, kidney and brain, can be affected and manifested with widespread inflammation and tissue damage. The accumulation of a wide spectrum of autoantibodies against self-nuclear components is a hallmark of SLE. 1 Follicular helper T (TFH) cells, a subset of CD4+ T helper (TH) cells, are required for the precise control of antibody production by germinal centre (GC) B cells. 2, 3 It is well-recognised that overexpansion or dysregulation of TFH cells is the root of the aberrant production of self-reactive antibodies that promote lupus pathogenesis. 4 Thus, a deeper understanding of the mechanisms controlling TFH cell differentiation and function may facilitate the development of therapies to treat SLE.Wu et al. have presented a new mechanism by which the TFH response is potentially dysregulated in SLE patients. The expression of Absent in melanoma 2 (human AIM2 and murine Aim2) is found to be increased in TFH-like cells (CD4+ Bcl6+ PD1+) in the peripheral blood and skin lesions of lupus patients, compared to healthy controls. The elevated AIM2 level is attributed to the increased recruitment of the hydroxymethyltransferase ten-eleven translocation