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This disparity is typically attributed to differences in neoantigen load. However, whether antigen-independent mechanisms contribute to immune evasion in MSS colorectal cancer remains unclear. To address this, we engineered a model in which MSI and MSS colorectal cancer cells express identical levels of a defined antigen recognized by T-cell receptor\u2013engineered T cells. Despite equivalent antigen presentation, MSS tumors exhibited impaired T-cell activation, reduced cytotoxicity, and resistance to killing. We linked this immune evasion to the MSS tumor secretome, which suppressed immune responses even in immunogenic MSI cells by impairing immune synapse formation. Surfaceome profiling by mass spectrometry identified glycosylation-dependent alterations that impair immune recognition. Our findings demonstrate that MSS colorectal cancer evades immune attack via intrinsic secretome-driven mechanisms, independent of antigenicity. Targeting glycosylation-linked suppressive pathways may restore T-cell responsiveness and improve immunotherapy efficacy in MSS colorectal cancer.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance:<\/jats:title>\n                    <jats:p>This study reveals that MMR-proficient colorectal cancers resist T-cell attack not only due to low neoantigen load but also through glycosylation-dependent, secretome-mediated immunosuppression. These findings uncover a previously unrecognized immune evasion mechanism and identify actionable pathways to restore immunotherapy responsiveness in resistant colorectal tumors.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1158\/2159-8290.cd-26-0542","type":"journal-article","created":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T13:01:13Z","timestamp":1778677273000},"page":"1992-2007","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Mismatch Repair\u2013Proficient Colorectal Cancer Can Evade Immune Surveillance through an Intrinsic Suppressive Program"],"prefix":"10.1158","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8168-8649","authenticated-orcid":false,"given":"Chiara Maria","family":"Cattaneo","sequence":"first","affiliation":[{"name":"1IRCCS Humanitas Research Hospital, Milan, Italy."},{"name":"2IFOM ETS\u2013The AIRC Institute of Molecular Oncology, Milan, 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Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7612-6097","authenticated-orcid":false,"given":"Zulma Irene","family":"Magnani","sequence":"additional","affiliation":[{"name":"4Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan, Italy."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1555-587X","authenticated-orcid":false,"given":"Wouter","family":"Scheper","sequence":"additional","affiliation":[{"name":"5Department of Molecular Oncology and Immunology, the Netherlands Cancer Institute, Amsterdam, the Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6841-4240","authenticated-orcid":false,"given":"Luca","family":"Lazzari","sequence":"additional","affiliation":[{"name":"2IFOM ETS\u2013The AIRC Institute of Molecular Oncology, Milan, 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