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However, the ICB\u2010resistant mechanisms remain largely unclear and require further investigation. Here, an immunosuppressive ecosystem in ICB\u2010resistant tumors is identified, featured by preferential infiltration of MARCO+ tumor\u2010associated macrophages (TAMs) and restrained cytotoxicity of CD8+ cytotoxic T lymphocytes (CTLs). The infiltrated MARCO+ TAMs can obstruct the development of CD8+ CTLs by impairing MHC\u2010I\u2010mediated neoantigen cross\u2010presentation. Mechanistically, MARCO up\u2010regulates the expression of SOCS1, which obstructs the kinase activity of JAK1, thereby downregulating MHC\u2010I expression through the inhibition of the JAK1\u2010STAT1\u2010NLRC5 signaling cascade. Further, MARCO blockade significantly facilitates ICB therapy in in vivo models by recovering tumor recognition and priming anti\u2010tumor CD8+ T cell responses. Taken together, these findings highlight MARCO as a highly desirable target in ICB\u2010refractory individuals for immunorecognition reignition and immunotherapy modulation.<\/jats:p>","DOI":"10.1002\/advs.202514600","type":"journal-article","created":{"date-parts":[[2025,10,21]],"date-time":"2025-10-21T09:00:06Z","timestamp":1761037206000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["MARCO+ Tumor\u2010Associated Macrophages Impede CD8+ T Cell Immunity to Facilitate Immunotherapy Resistance in Renal Cell Carcinoma"],"prefix":"10.1002","volume":"12","author":[{"given":"Jiayuan","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Genitourinary Oncology Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education\/Beijing) Peking University Cancer Hospital &amp; Institute Peking University  Beijing 100142 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