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    CD24-Siglec axis is an innate immune checkpoint against metaflammation and metabolic disorder.

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    Author
    Wang, Xu
    Liu, Mingyue
    Zhang, Jifeng
    Brown, Nicholas K
    Zhang, Peng
    Zhang, Yan
    Liu, Heng
    Du, Xuexiang
    Wu, Wei
    Devenport, Martin
    Tao, Weng
    Mao-Draayer, Yang
    Chen, Guo-Yun
    Chen, Y Eugene
    Zheng, Pan
    Liu, Yang
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    Date
    2022-08-02
    Journal
    Cell Metabolism
    Publisher
    Elsevier
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1016/j.cmet.2022.07.005
    Abstract
    The molecular interactions that regulate chronic inflammation underlying metabolic disease remain largely unknown. Since the CD24-Siglec interaction regulates inflammatory response to danger-associated molecular patterns (DAMPs), we have generated multiple mouse strains with single or combined mutations of Cd24 or Siglec genes to explore the role of the CD24-Siglec interaction in metaflammation and metabolic disorder. Here, we report that the CD24-Siglec-E axis, but not other Siglecs, is a key suppressor of obesity-related metabolic dysfunction. Inactivation of the CD24-Siglec-E pathway exacerbates, while CD24Fc treatment alleviates, diet-induced metabolic disorders, including obesity, dyslipidemia, insulin resistance, and nonalcoholic steatohepatitis (NASH). Mechanistically, sialylation-dependent recognition of CD24 by Siglec-E induces SHP-1 recruitment and represses metaflammation to protect against metabolic syndrome. A first-in-human study of CD24Fc (NCT02650895) supports the significance of this pathway in human lipid metabolism and inflammation. These findings identify the CD24-Siglec-E axis as an innate immune checkpoint against metaflammation and metabolic disorder and suggest a promising therapeutic target for metabolic disease.
    Rights/Terms
    Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
    Keyword
    CD24
    NASH
    Siglec-E
    Siglecs
    insulin resistance
    metabolic syndrome
    metaflammation
    obesity
    sialic acid-binding immunoglobulin-like lectins
    sialylation
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/19547
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.cmet.2022.07.005
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