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The parasite's surface is covered by a dense glycocalyx enriched in GPI\u2010anchored mucins, trans\u2010sialidases, and glycoinositolphospholipids (GIPLs), which collectively shape host\u2013parasite interactions. Here we synthesize structural and biosynthetic features of key glycoconjugates and discuss how they modulate innate and adaptive immunity through pattern\u2010recognition receptors (e.g., TLR2\/6 and TLR4), inhibitory lectins (e.g., Siglec\u2010E), extracellular vesicle signalling, and complement evasion mediated by TS\u2010like regulators (T\u2010DAF, TcCRP) and factor H recruitment. We highlight how strain\u2010 and stage\u2010specific glycan variation, including \u03b1\u2010Gal\n                    <jats:italic>p<\/jats:italic>\n                    \u2010 and \u03b2\u2010Gal\n                    <jats:italic>f<\/jats:italic>\n                    \u2010containing epitopes, influences immune recognition, pathogenesis, and persistence. Finally, we evaluate translational opportunities: parasite\u2010selective targeting of sugar\u2010nucleotide metabolism and glycosyltransferases, and development of defined glycoepitopes (glycotopes) as improved biomarkers for diagnosis and post\u2010treatment monitoring. Together, these insights position the\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>T. cruzi<\/jats:italic>\n                    <\/jats:styled-content>\n                    glycocalyx as a central driver of immunomodulation and a promising source of therapeutic, vaccine and diagnostic targets.\n                  <\/jats:p>","DOI":"10.1111\/pim.70092","type":"journal-article","created":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T13:42:56Z","timestamp":1783690976000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Glycocalyx\u2010Driven Immunomodulation in\n                    <i>Trypanosoma cruzi<\/i>\n                    : Structures, Host Responses, Diagnostic and Therapeutic Targeting"],"prefix":"10.1111","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0154-7406","authenticated-orcid":false,"given":"Norton","family":"Heise","sequence":"first","affiliation":[{"name":"Instituto de Biof\u00edsica Carlos Chagas Filho Universidade Federal do Rio de Janeiro  Rio de Janeiro Brazil"},{"name":"Instituto Nacional de Ci\u00eancia e Tecnologia: Glicosa\u00fade  Rio de Janeiro Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher Mark","family":"West","sequence":"additional","affiliation":[{"name":"Department of Biochemistry &amp; Molecular Biology Center for Molecular Medicine, Center for Tropical and Emerging Global Diseases, University of Georgia  Athens Georgia USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1919-7582","authenticated-orcid":false,"given":"Carolina Macedo","family":"Koeller","sequence":"additional","affiliation":[{"name":"Instituto de Biof\u00edsica Carlos Chagas Filho Universidade Federal do Rio de Janeiro  Rio de Janeiro Brazil"},{"name":"Instituto Nacional de Ci\u00eancia e Tecnologia: Glicosa\u00fade  Rio de Janeiro Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,10]]},"reference":[{"key":"e_1_2_14_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fpubh.2019.00166"},{"key":"e_1_2_14_3_1","unstructured":"DNDi \u201cDisease Factsheet 2023\u201d(2023) 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