{
  "abstract": "Introduction: SARS-CoV-2 infections causing severe COVID-19 are known to induce or exacerbate thyroid dysfunctions (TD), comprising autoimmune thyroiditis and subacute thyroiditis. Non-thyroidal illness syndrome is also common. Thyroid damage could result from direct viral infection and/or aberrant immuno-inflammatory responses. However, the specific immunological mechanisms contributing to TD in severe COVID-19 are not fully understood.\n\nMethods: We investigated the relationship between severe SARS-CoV-2 infection and TD by analyzing antibody autoreactivity and fucosylation level in 40 COVID-19 patients recruited during the 2020 pandemic wave. Using protein arrays, ELISA, and computational modeling, we compared patients with and without TD to 20 healthy controls and 29 Graves’ disease cases, focusing on the functional impact of the elicited antibodies.\n\nResults: We observed a significant shift in IgG autoreactivity, specifically targeting CD16A and KIR2DL1 in COVID-19 patients, both TD and not-TD, compared to Healthy Controls (HC) or other thyroid disease patients. Anti-Spike IgGs from COVID-19-TD patients exhibited a lower fucosylation state compared with those without TD and were associated with increased NK-cell activation and degranulation. Furthermore, patients’ sera showed increased binding to immortalized human thyroid epithelial cells. Computational analysis identified structural similarities between the SARS-CoV-2 Spike protein and thyroglobulin.\n\nDiscussion: Thyroid damage in severe COVID-19 involves a complex interplay of different mechanisms. We proposed a potential role of lowly fucosylated anti-Spike antibodies, which may contribute to heightened NK cell-mediated activation via CD16A, potentially exacerbated by virus-induced autoreactivity. Altered IgG fucosylation and autoreactivity are associated with thyroid dysfunctions in severe COVID-19.",
  "abstract_shown": true,
  "affiliations": [
    "Istituto Nazionale di Genetica Molecolare (INGM) “Romeo ed Enrica Invernizzi”",
    "Department of Clinical Sciences and Community Health, Department of Excellence 2023-2027, University of Milan",
    "Department of Chemistry, University of Pavia",
    "CheckmAb SrL",
    "Infectious Diseases Unit, Foundation IRCCS Ca’ Granda Ospedale Maggiore Policlinico",
    "Department of Pathophysiology and Transplantation, University of Milan",
    "Endocrinology Unit, Graves’ Orbitopathy Center, Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 17,
  "authors": [
    {
      "affs": [
        0,
        1
      ],
      "name": "Elisa Pesce"
    },
    {
      "affs": [
        0
      ],
      "name": "Andrea Gobbini"
    },
    {
      "affs": [
        0
      ],
      "name": "Mauro Bombaci"
    },
    {
      "affs": [
        0
      ],
      "name": "Andrea Favalli"
    },
    {
      "affs": [
        1
      ],
      "name": "Sara Maioli"
    },
    {
      "affs": [
        2
      ],
      "name": "Stefano Artin Serapian"
    },
    {
      "affs": [
        3
      ],
      "name": "Noemi di Marzo"
    },
    {
      "affs": [
        3
      ],
      "name": "Luca Sorrentino"
    },
    {
      "affs": [
        3
      ],
      "name": "Mirco Toccafondi"
    },
    {
      "affs": [
        0
      ],
      "name": "Paola Gruarin"
    },
    {
      "affs": [
        4,
        5
      ],
      "name": "Andrea Lombardi"
    },
    {
      "affs": [
        1,
        6
      ],
      "name": "Mirco Armenti"
    },
    {
      "affs": [
        0
      ],
      "name": "Mariangela Lorenzo"
    },
    {
      "affs": [
        4,
        5
      ],
      "name": "Alessandra Bandera"
    },
    {
      "affs": [
        2
      ],
      "name": "Giorgio Colombo"
    },
    {
      "affs": [
        1,
        6
      ],
      "name": "Ilaria Muller"
    },
    {
      "affs": [
        0
      ],
      "name": "Renata M. Grifantini"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/2zh2axttz9k53.bib",
  "cited_by": 0,
  "doi": "10.3389/fimmu.2026.1806272",
  "fulltext_url": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13724446/?tool=EBI",
  "id": "2zh2axttz9k53",
  "issns": [
    "1664-3224"
  ],
  "landing_url": "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1806272/full",
  "language": "eng",
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "Original Research"
    ],
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      "openalex",
      "2712|Thyroid Disorders and Treatments"
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  "openalex": "W7222962490",
  "pdf_url": "https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2026.1806272/pdf",
  "pmcid": "PMC13724446",
  "pmid": "42973736",
  "published": "2026-10-19",
  "publisher": "Frontiers Media SA",
  "ris": "https://research.draconitic.com/paper/2zh2axttz9k53.ris",
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  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2712|Thyroid Disorders and Treatments",
      "subfield": "endocrinology-metabolism"
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  ],
  "title": "Antibody afucosylation and enhanced autoreactive antibody response are associated with thyroid dysfunction during severe SARS-CoV-2 infection",
  "title_text": "Antibody afucosylation and enhanced autoreactive antibody response are associated with thyroid dysfunction during severe SARS-CoV-2 infection",
  "type": "peer-reviewed",
  "updated_at": "2026-11-05T12:21:12Z",
  "url": "https://research.draconitic.com/paper/2zh2axttz9k53",
  "venue": "Frontiers in Immunology",
  "versions": []
}