FCER1G

更新于：2025-05-07

基本信息

别名

Fc epsilon receptor Ig、Fc fragment of IgE receptor Ig、Fc fragment of IgE, high affinity I, receptor for; gamma polypeptide

+ [8]

简介

Adapter protein containing an immunoreceptor tyrosine-based activation motif (ITAM) that transduces activation signals from various immunoreceptors. As a component of the high-affinity immunoglobulin E (IgE) receptor, mediates allergic inflammatory signaling in mast cells. As a constitutive component of interleukin-3 receptor complex, selectively mediates interleukin 4/IL4 production by basophils, priming T-cells toward effector T-helper 2 subset. Associates with pattern recognition receptors CLEC4D and CLEC4E to form a functional signaling complex in myeloid cells. Binding of mycobacterial trehalose 6,6'-dimycolate (TDM) to this receptor complex leads to phosphorylation of ITAM, triggering activation of SYK, CARD9 and NF-kappa-B, consequently driving maturation of antigen-presenting cells and shaping antigen-specific priming of T-cells toward effector T-helper 1 and T-helper 17 cell subtypes. May function cooperatively with other activating receptors. Functionally linked to integrin beta-2/ITGB2-mediated neutrophil activation. Also involved in integrin alpha-2/ITGA2-mediated platelet activation.

关联

100 项与 FCER1G 相关的临床结果

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100 项与 FCER1G 相关的转化医学

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0 项与 FCER1G 相关的专利（医药）

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520

项与 FCER1G 相关的文献（医药）

2025-05-01·Reproductive Toxicology

Identification of endocrine disrupting chemicals targeting NTD-related hub genes during pregnancy via in silico analysis

Article

作者: Chen, Yuzhu ; Liu, Jinming ; Yu, Hao ; Guo, Yujun ; Li, Zhaozhu ; Guo, Junjie

Neural tube defects (NTDs) represent severe congenital malformations of the central nervous system with multifactorial etiology, involving intricate gene-environment interactions that remain incompletely characterized. Endocrine disrupting chemicals (EDCs) are exogenous substances with hormone-disrupting properties that are ubiquitous in our surroundings. These chemicals pose a significant threat to human health, contributing to a range of diseases. Pregnant women are particularly vulnerable to the effects of EDCs, as these substances can traverse the placental barrier and impact the development of both the placenta and fetus. This study utilized placental and fetal transcriptome data to identify hub genes associated with NTDs during pregnancy. By leveraging the Comparative Toxicogenomics Database (CTD), we predicted the EDCs targeting these hub genes and performed molecular docking to assess their interactions. Our findings revealed four hub genes (CTSC, FCER1G, ITGB2, and LYVE1) in NTDs, with 72 EDCs identified as their targets. Molecular docking demonstrated that atrazine, bisphenol A (BPA) and diuron exhibited stable affinity with the proteins encoded by hub genes. These findings provide new insights into the environmental endocrine disruptors that affect the development of NTDs during pregnancy.

2025-04-11·Science Immunology

Bcl11a maintains hematopoietic stem cell function but accelerates inflammation-driven exhaustion during aging

Article

作者: Jiang, Cizhong ; Li, Kairui ; Xu, Xiang ; Guo, Rui ; Zhang, Li ; Cui, Xinyu ; Wang, Jing ; Yu, Yong ; Zhang, Linlin ; Xu, Bing

Preserving hematopoietic stem cell (HSC) functionality is essential for maintaining healthy blood and the immune system throughout life. HSC function declines with age; however, the underlying mechanisms are not fully understood. Using an inducible mosaic mouse model to overexpress the transcription factor Bcl11a in the hematopoietic compartment, we found that an aging-related increase in Bcl11a mitigated HSC functional decline, promoted IL-1β production in the bone marrow (BM), and accelerated HSC attrition in a non–cell-autonomous manner. Aging-related inflammation in the BM enhanced Bcl11a and Fc receptor (FcR) expression in HSCs, and FcR signaling induced HSC differentiation. This was counteracted by Bcl11a through repression of Fcer1g . Bcl11a up-regulation promoted IL-1β production in BM myeloid cells, driving inflammation and HSC deterioration. Deletion of Fcer1g , or blocking IL-1β signaling, eliminated this non–cell-autonomous effect on HSC decline. These findings demonstrate that Bcl11a plays a dual role in HSCs during aging not only by cell-intrinsically preserving HSC function but also by promoting BM inflammation and HSC dysfunction.

2025-04-01·Allergology International

Elevated MS4A2 and IgE interaction in nasal polyps contributing to poor postoperative prognosis in patients with eosinophilic chronic rhinosinusitis

Article

作者: Hatano, Akihiro ; Okada, Naoko ; Yoshikawa, Mamoru ; Inoue, Natsuki ; Yamaguchi, Sota ; Inoue, Hiroko ; Nakano, Mika

BACKGROUNDChronic rhinosinusitis (CRS) is a persistent inflammatory disease of various endotypes, including eosinophilic CRS (eCRS), which is characterized by marked eosinophilic infiltration and high refractory rates despite treatment. Recent findings suggest the interaction between local IgE and mast cells in nasal polyps (NPs) is key to eCRS pathogenesis; however, the details remain unclear. This study investigated the involvement of MS4A2, a component of the IgE receptor, in the pathogenesis of refractory eCRS.METHODSNP tissue samples were collected from 47 patients with eCRS who underwent sinus surgery and classified into refractory and nonrefractory groups based on postoperative outcomes. Quantitative PCR was used to analyze the mRNA expression of IgE receptor components (MS4A2, FCER1A, and FCER1G) and cell-specific markers (CLC, TPSAB1, and GPR56) in NP tissues. Immunofluorescence staining was used to confirm MS4A2 expression and colocalization with tryptase, ProMBP1, and IgE. ROC analysis was conducted to assess MS4A2 mRNA levels as a predictor of refractory eCRS.RESULTSMS4A2 mRNA expression was significantly elevated in the refractory group, whereas FCER1A and FCER1G mRNA expression levels showed no significant differences. Immunofluorescence revealed an increased number of MS4A2-positive cells, particularly those colocalized with tryptase-positive mast cells, in the refractory group. Cells coexpressing MS4A2 and IgE were more prevalent in this group. ROC analysis indicated that MS4A2 mRNA expression can predict prognosis with high specificity.CONCLUSIONSOur findings suggest the significance of the interaction between MS4A2-expressing mast cells and local IgE in the pathogenesis of refractory eCRS, highlighting MS4A2 as a potential therapeutic target.

项与 FCER1G 相关的新闻（医药）

2025-04-20

·微信

逆转血液衰老！同济大学团队发现关键衰老调控机制

近日，同济大学生命科学与技术学院余勇教授团队与江赐忠教授团队合作，在《科学-免疫学》（Science Immunology）发表研究论文，通过创新性构建诱导型Bcl11a嵌合小鼠模型，结合多组学测序与功能验证，首次系统解析了转录因子Bcl11a在造血干细胞（HSC）稳态与衰老进程中的双重调控机制，为血液系统衰老干预提供了重要理论突破。随着年龄增长，造血干细胞（HSC）功能衰退，导致血液和免疫系统功能下降，但其具体机制一直是个谜。研究团队发现，随着年龄增长，HSC中Bcl11a的表达水平显著上升。为深入研究其功能，团队构建了一种特殊的嵌合小鼠模型，能够在特定条件下诱导Bcl11a过表达。通过竞争性移植实验和免疫荧光染色技术，团队在同一骨髓微环境中对比了Bcl11a过表达HSCs与正常HSCs的功能。结果表明，Bcl11a过表达不仅显著增强了HSCs的造血能力，还延缓了其衰老进程，而与之共存的正常HSCs则表现出明显的功能退化。为揭示Bcl11a的作用机制，研究团队运用先进的CUT&Tag技术绘制了Bcl11a全基因组结合图谱，并整合了转录组（RNA-Seq）及染色质可及性（ATAC-Seq）数据分析。研究发现Bcl11a能够特异性抑制Fc受体信号通路中的关键基因Fcer1g。进一步的功能实验证实，Fcer1g信号通路的激活会触发HSCs内炎症相关网络的活化，导致干细胞分化加速和自我更新能力受损。这一发现揭示了Bcl11a通过抑制Fcer1g来维持HSCs静息态的核心机制，从而在造血稳态及应激条件下有效增强HSCs功能，延缓衰老相关的功能衰退。▲研究示意图（图片来源：原始论文[1]）然而，研究团队发现Bcl11a过表达在衰老过程中呈现“双刃剑”效应：在增强HSCs功能的同时，显著促进了骨髓髓系细胞的异常增殖，导致骨髓微环境中IL-1β水平持续升高。这种慢性炎症状态通过激活正常HSCs表面的Fc受体，最终引发干细胞功能耗竭。团队通过使用IL-1β受体拮抗剂或敲除Fcer1g基因，成功逆转了HSCs的功能衰退，证实IL-1β-Fcer1g轴是介导HSCs非自主性耗竭的核心分子通路。该研究首次阐明了Bcl11a在HSC衰老中的双重调控机制：一方面通过维持HSC静息态抵抗内源性衰老，另一方面却通过诱导炎症微环境加速外源性耗竭。该研究不仅加深了我们对HSCs衰老机制的理解，还为延缓衰老相关的血液系统疾病（如免疫力下降、血液肿瘤风险增加等）提供了新的潜在靶点。同济大学生命科学与技术学院余勇教授、江赐忠教授为论文共同通讯作者。同济大学生命科学与技术学院王晶博士、张林林博士研究生、崔昕宇博士、徐香博士研究生为论文共同第一作者。该研究得到了同济大学高绍荣教授、梁爱斌教授和香港大学刘澎涛教授的大力支持与帮助。文章来源：同济大学原始论文：[1] Bcl11a maintains hematopoietic stem cell function but accelerates inflammation-driven exhaustion during aging. Science Immunology (2025). DOI: 10.1126/sciimmunol.adr2041免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。更多推荐点个“在看”再走吧~

放射疗法

2022-09-09

·佰傲谷BioValley

肿瘤免疫治疗新秀：天然免疫样CD8+T细胞

在最近发表在《自然》杂志发表了一项研究，Chou和他的同事定义了一种新型抗肿瘤T细胞亚群：进化上保守，表达αβTCR和FCER1G，具有高细胞毒性和天然免疫细胞（NK1.1）特征，命名为αβILTCKs。αβILTCKs：抗肿瘤活性为了全面表征肿瘤浸润性细胞毒性T细胞的表型，Chou和同事直接从MMTV-PyMT(PyMT)小鼠乳腺癌组织中分离的CD45+TCRβ+CD8α+细胞进行单细胞RNA测序分析。生物信息学聚类鉴定了五种不同的T细胞群，包括初始T细胞、激活T细胞、耗竭T细胞、增殖T细胞，以及以高表达NK1.1的αβILTCKs。这些细胞具有独特的转录组，不同于传统的肿瘤浸润CD8+T细胞。它们属于非传统的1型样先天淋巴样细胞。同一研究组之前的工作表明，αβILTCKs原则上可以对肿瘤细胞表现出固有的细胞毒性。天然免疫与肿瘤免疫监视（Cell，2016）Chou和同事还在小鼠前列腺癌和人类结直肠癌组织中检测到αβILTCKs，表明它们可能代表了进化上保守的肿瘤诱导免疫监测调节因子。与经典的PD1+TCR+CD8+T细胞祖细胞不同比较了来自肿瘤驻留的NK1.1+CD8α+αβILTCKs和传统的PD-1+CD8α+T细胞(PD-1+T细胞)的配对TCR序列，这两个肿瘤浸润性T细胞亚群并不是来源于共同的祖细胞，而是代表了两个完全不同的祖细胞。与PD1+TCR+CD8+T细胞识别肿瘤抗原不同针对PD-1轴的免疫治疗，需要传统的PD-1+T细胞的活性，这些传统的CTLs通常识别具有高肿瘤突变负担的肿瘤，因为它们的TCR能够检测到突变的新抗原是“非自身”。相比之下，NK1.1+CD8α+αβILTCKs的大多数TCR识别未突变癌症特异性肽。特异性表达FCER1G将肿瘤浸润αβILTCKs的基因表达谱与PyMT小鼠乳腺肿瘤组织中所有其他CD45+TCRβ+CD8α+细胞的基因表达谱进行了比较。编码Fc Epsilon受体Ig蛋白(FCER1G)的Fcer1g的表达与其他肿瘤浸润CD8+T细胞，包括PD-1+T细胞相比有显著差异，无论它们的激活状态如何。在原发性人类结肠癌组织中，在TCRβ+细胞中也检测到FCER1G的表达，其共受体表达谱与小鼠αβILTCK相似。此外，与邻近的正常组织相比，这些FCER1G+T细胞在癌变组织中富集，表明FCER1G是一个谱系定义的标志物，是肿瘤浸润T细胞进入αβILTCK谱系的特征。Signal Transduct Target Ther. 2022.抗肿瘤活性依赖IL-15在S100a8-cre-Il15fl/fl PyMT小鼠模型中，癌细胞来源的IL-15丢失导致肿瘤组织中αβILTCK招募减少，癌症免疫监测受损，与野生型对照相比，肿瘤生长加速。接下来，作者通过在αβILTCK祖细胞中选择性地表达功能获得的STAT5B变体(STAT5B-CA)，组成性激活IL-15R信号通路。将这些工程αβILTCKs过继转移到淋巴细胞缺陷的肿瘤携带PyMT小鼠中，与对照组αβILTCKs相比，强烈抑制了肿瘤生长。简评：αβILTCKs表达的PD-1下降，因而PD-（L）1抑制剂对此群细胞可能无效。αβILTCKs和经典的PD-1+T细胞互补，识别未突变的肿瘤抗原，且依赖于IL-15信号，为联用IL-15和PD-1抑制剂提供了理论基础。近期热门视频更多精彩视频，尽在佰傲谷视频号，欢迎关注~本周好文推荐如需转载请联系佰傲谷并在醒目位置注明出处﹀点亮在看，传递信息♥

免疫疗法细胞疗法抗体