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The GAS Rgg2\/Rgg3 quorum-sensing (QS) system, a cell-to-cell communication network, modifies the cell surface, resulting in increased lysozyme resistance, biofilm formation, and expression of the\n                      <jats:italic toggle=\"yes\">qim<\/jats:italic>\n                      operon which is responsible for modulation of innate immune responses in macrophages. The operon encodes 10 genes with predicted homology to enzymes involved in bacterial cell surface-associated carbohydrate and teichoic acid biosynthesis pathways. Comparing extracts of GAS cell wall polysaccharides between wild type and operon mutants showed that QS-induced genes modify the\n                      <jats:italic toggle=\"yes\">S. pyogenes<\/jats:italic>\n                      cell surface by adding a wall teichoic acid-like\n                      <jats:italic toggle=\"yes\">N<\/jats:italic>\n                      -acetylglucosamine-linked ribitol (GlcNAc-Rbo) moiety. A fluorescently labeled phage receptor-binding protein, RBP-13-GFP, that recognizes GlcNAc-decorated ribitol phosphate repeats, bound to the GAS surface only when\n                      <jats:italic toggle=\"yes\">qim<\/jats:italic>\n                      expression was induced. Deletion of the\n                      <jats:italic toggle=\"yes\">qim<\/jats:italic>\n                      operon eliminated RBP-13-GFP binding, diminished bacterial colonization, and significantly attenuated GAS pathogenesis in a murine skin infection model. These findings indicate that GAS has evolved a strategy to evade innate immune response by presenting a previously unknown carbohydrate moiety upon QS.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Streptococcus pyogenes<\/jats:italic>\n                        is a major human pathogen, responsible for diverse clinical manifestations of both superficial and invasive infections, and can lead to post-infection sequelae like rheumatic heart disease, whose prevalence on a global scale rivals that of the most serious pathogens. Invasive\n                        <jats:italic toggle=\"yes\">S. pyogenes<\/jats:italic>\n                        infections are currently on the rise worldwide, notably correlating with increasing pediatric cases of scarlet fever and enhancing the concern for long-term complications. There is much that remains unknown about\n                        <jats:italic toggle=\"yes\">S. pyogenes<\/jats:italic>\n                        virulence and pathogenicity, and studies focused on understanding basic systems regulating virulence factors could lead to better therapeutics and translational research. We show here one such example, where a bacterial communication system regulating a virulence mechanism relevant to\n                        <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                        infection confers the ability to alter the host\u2019s innate immune response. We find that modifications to the cell wall arise when this virulence system is activated, which has a direct role in host-pathogen interactions. Further research into this system could provide a mechanism for disruption and serve to treat\n                        <jats:italic toggle=\"yes\">S. pyogenes<\/jats:italic>\n                        infection.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.03801-25","type":"journal-article","created":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T14:00:32Z","timestamp":1771941632000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["A teichoic acid-like wall modification associated with immune suppression is socially regulated in\n                    <i>Streptococcus pyogenes<\/i>"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3395-7805","authenticated-orcid":true,"given":"Caleb 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