{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T23:56:25Z","timestamp":1792799785981,"version":"4.5.0"},"reference-count":68,"publisher":"American Society for Clinical Investigation","issue":"24","license":[{"start":{"date-parts":[[2024,12,16]],"date-time":"2024-12-16T00:00:00Z","timestamp":1734307200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH, Novo Nordisk Foundation","award":["National Institute of Health (grants R01AI127406,R01AI144694"],"award-info":[{"award-number":["National Institute of Health (grants R01AI127406,R01AI144694"]}],"id":[{"id":"https:\/\/ror.org\/04txyc737","id-type":"ROR","asserted-by":"crossref"}]},{"name":"NIH, Novo Nordisk Foundation","award":["R35 GM119850)"],"award-info":[{"award-number":["R35 GM119850)"]}],"id":[{"id":"https:\/\/ror.org\/04txyc737","id-type":"ROR","asserted-by":"crossref"}]},{"name":"NIH, Novo Nordisk Foundation","award":["the Novo Nordisk Foundation (NNF20SA0066621)"],"award-info":[{"award-number":["the Novo Nordisk Foundation (NNF20SA0066621)"]}],"id":[{"id":"https:\/\/ror.org\/04txyc737","id-type":"ROR","asserted-by":"crossref"}]},{"name":"national institute of health","award":["R01AI179098"],"award-info":[{"award-number":["R01AI179098"]}]},{"name":"National institute of Health","award":["R01AI181321"],"award-info":[{"award-number":["R01AI181321"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,12,16]]},"abstract":"<jats:p>\n                    The pathobiont\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-\u03b12,3sialylation of antibodies and loss of protective activity. IL-10 enhances \u03b12,3sialylation on cell-wall\u2013associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti\u2013\n                    <jats:italic>Streptococcus pyogenes<\/jats:italic>\n                    and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy.\n                  <\/jats:p>","DOI":"10.1172\/jci179563","type":"journal-article","created":{"date-parts":[[2024,12,15]],"date-time":"2024-12-15T14:00:43Z","timestamp":1734271243000},"source":"Crossref","is-referenced-by-count":15,"title":["Pathobiont-driven antibody sialylation through IL-10 undermines vaccination"],"prefix":"10.1172","volume":"134","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7305-7401","authenticated-orcid":true,"given":"Chih-Ming","family":"Tsai","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Pediatrics, University of California, La Jolla, California, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irshad A.","family":"Hajam","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Pediatrics, 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