Leukocyte immunoglobulin‐like receptor A3 is increased in IBD patients and functions as an anti‐inflammatory modulator,Clinical & Experimental Immunology

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Leukocyte immunoglobulin‐like receptor A3 is increased in IBD patients and functions as an anti‐inflammatory modulator
Clinical & Experimental Immunology ( IF 3.4 ) Pub Date : 2020-10-02 , DOI: 10.1111/cei.13529
X Lan ₁ , F Liu ₂ , J Ma ₃ , Y Chang ₄ , X Lan ₅ , L Xiang ₆ , X Shen ₁ , F Zhou ₄ , Q Zhao ₄

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Growing evidence shows that a homozygous 6·7‐kb deletion of the novel anti‐inflammatory molecule leukocyte immunoglobulin‐like receptor A3 (LILRA3) is associated with many autoimmune disorders. However, its effects on pathogenesis of inflammatory bowel disease (IBD) have yet not been clarified. LILRA3 is mainly expressed in monocytes, whereas its effects on biological behaviors of monocytes have not been systematically reported. In our study, to investigate the association between LILRA3 polymorphism and IBD susceptibility, LILRA3 polymorphism was assessed in 378 IBD patients and 509 healthy controls. Quantitative real time PCR (qRT–PCR), Western blot and immunohistochemistry (IHC) were employed to detect the LILRA3 expression in IBD patient blood and intestinal samples. The human U937 monocyte cell line was employed to establish LILRA3 over‐expressing cells and the effects of LILRA3 on the biological behaviors of U937 cells were systematically explored. Although no association of the polymorphism with IBD development was found, LILRA3 expression was markedly increased in IBD patients compared with healthy controls. Over‐expression of LILRA3 in monocytes led to significant decreases in secretion of interferon (IFN)‐γ, tumor necrosis factor (TNF)‐α and interleukin (IL)‐6. Additionally, LILRA3 abated monocyte migration by reducing the expression of several chemokines and enhanced monocyte phagocytosis by increasing CD36 expression. Furthermore, LILRA3 promoted monocyte proliferation through a combination of Akt and extracellular receptor kinase/mitogen‐activated protein kinase (Erk/MEK) signaling pathways. We report for the first time, to our knowledge, that LILRA3 is related to IBD and functions as an anti‐inflammatory modulator in U937 cells.

中文翻译：

白细胞免疫球蛋白样受体 A3 在 IBD 患者中增加并起到抗炎调节剂的作用

越来越多的证据表明，新型抗炎分子白细胞免疫球蛋白样受体 A3 (LILRA3) 的纯合 6·7-kb 缺失与许多自身免疫性疾病有关。然而，其对炎症性肠病（IBD）发病机制的影响尚未阐明。LILRA3主要在单核细胞中表达，其对单核细胞生物学行为的影响尚未系统报道。在我们的研究中，为了调查 LILRA3 多态性与 IBD 易感性之间的关联，在 378 名 IBD 患者和 509 名健康对照中评估了 LILRA3 多态性。采用实时定量 PCR (qRT-PCR)、蛋白质印迹和免疫组织化学 (IHC) 检测 IBD 患者血液和肠道样本中 LILRA3 的表达。采用人U937单核细胞系建立LILRA3过表达细胞，系统探讨了LILRA3对U937细胞生物学行为的影响。尽管未发现多态性与 IBD 发展相关，但与健康对照相比，IBD 患者的 LILRA3 表达显着增加。LILRA3 在单核细胞中的过度表达导致干扰素 (IFN)-γ、肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-6 的分泌显着减少。此外，LILRA3 通过减少几种趋化因子的表达来减少单核细胞迁移，并通过增加 CD36 表达来增强单核细胞吞噬作用。此外，LILRA3 通过 Akt 和细胞外受体激酶/丝裂原活化蛋白激酶 (Erk/MEK) 信号通路的组合促进单核细胞增殖。

更新日期：2020-10-02

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