Publication

Innate immune Galectin-7 specifically targets microbes that decorate themselves in blood-like

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Last modified
  • 05/22/2025
Type of Material
Authors
    Shang-Chuen Wu, Harvard Medical SchoolNourine A Kamili, Harvard Medical SchoolMarcelo Dias-Baruffi, Univ Sao PauloCassandra Josephson, Emory UniversityMatthew F Rathgeber, Harvard Medical SchoolMelissa Y Yeung, Harvard Medical SchoolWilliam J Lane, Harvard Medical SchoolJianmei Wang, Emory UniversityHau-Ming Jan, Harvard Medical SchoolSeth Rakoff-Nahoum, Harvard Medical SchoolRichard Cummings, Emory UniversitySean Stowell, Emory UniversityConnie M Arthur, Harvard Medical School
Language
  • English
Date
  • 2022-07-15
Publisher
  • CELL PRESS
Publication Version
Copyright Statement
  • © 2022 The Author(s)
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Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 25
Issue
  • 7
Start Page
  • 104482
End Page
  • 104482
Grant/Funding Information
  • This work was supported by grants from the US National Institutes of Health to R.D.C. (HL085607 and R24 GM137763) and by resources from the Consortium for Functional Glycomics (Core D and Core H), funded by the US National Institute of General Medical Sciences/U.S. National Institutes of Health (GM62116) and the Burroughs Wellcome Trust Career Award for Medical Scientists, the National Institutes of Health Early Independence grant DP5OD019892, and U01 CA242109 to SRS.
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Abstract
  • Adaptive immunity can target a nearly infinite range of antigens, yet it is tempered by tolerogenic mechanisms that limit autoimmunity. Such immunological tolerance, however, creates a gap in adaptive immunity against microbes decorated with self-like antigens as a form of molecular mimicry. Our results demonstrate that the innate immune lectin galectin-7 (Gal-7) binds a variety of distinct microbes, all of which share features of blood group-like antigens. Gal-7 binding to each blood group expressing microbe, including strains of Escherichia coli, Klebsiella pneumoniae, Providencia alcalifaciens, and Streptococcus pneumoniae, results in loss of microbial viability. Although Gal-7 also binds red blood cells (RBCs), this interaction does not alter RBC membrane integrity. These results demonstrate that Gal-7 recognizes a diverse range of microbes, each of which use molecular mimicry while failing to induce host cell injury, and thus may provide an innate form of immunity against molecular mimicry.
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Research Categories
  • Health Sciences, Medicine and Surgery

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