{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T14:01:37Z","timestamp":1790085697153,"version":"4.0.1"},"reference-count":251,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:00Z","timestamp":1790035200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Innate immune signaling is a central regulator of cancer immunity, but its effects are highly context-dependent. Acute and spatially controlled innate immune activation can promote dendritic-cell maturation, antigen presentation, and cytotoxic lymphocyte recruitment. In contrast, chronic, systemic, or therapy-induced inflammatory signaling often redirects the tumor ecosystem toward suppressive myeloid remodeling. This review discusses how innate immune pathways reshape myelopoiesis, macrophage polarization, MDSC activation, tumor-associated neutrophil recruitment, and stromal\u2013myeloid inflammatory niches. We focus on selected signaling axes that represent distinct layers of innate inflammatory regulation, including cytokine-mediated myeloid instruction, inflammasome activation, nucleic-acid sensing, chemokine-driven recruitment, stromal transcriptional integration, and lipid-mediator signaling. These axes include IL-4\/IL-4R\u03b1, IL-1\u03b1\/IL-1\u03b2, TGF-\u03b2, interferon signaling, NLRP3 inflammasome activation, STING, STAT3, IL-8\/CXCR2, CCR2, and CysLTR1. These pathways can expand suppressive myeloid output from the bone marrow, reinforce tumor-associated macrophage states such as TREM2\n                    <jats:sup>+<\/jats:sup>\n                    , SPP1\n                    <jats:sup>+<\/jats:sup>\n                    , and NLRP3\n                    <jats:sup>+<\/jats:sup>\n                    macrophages, and promote MDSC- and neutrophil-mediated resistance to immune checkpoint blockade. We also summarize tissue, spatial, and peripheral biomarkers that may identify myeloid-dominant immune resistance. Finally, we discuss therapeutic strategies aimed at blocking inflammatory drivers, inhibiting inflammasome-dependent amplification, preventing suppressive myeloid recruitment, and reprogramming established myeloid niches. Rather than cataloguing individual myeloid subsets or isolated inflammatory pathways, this review integrates systemic myelopoiesis, local TAM\/MDSC\/TAN remodeling, stromal\u2013myeloid spatial niches, and therapy-induced inflammatory feedback into a unified framework for understanding and targeting immune checkpoint blockade resistance.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1941227","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T13:15:32Z","timestamp":1790082932000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Innate immune signaling\u2013driven myeloid remodeling in cancer: inflammatory amplification, immune suppression, and therapeutic targeting"],"prefix":"10.3389","volume":"17","author":[{"given":"Wenyi","family":"Ye","sequence":"first","affiliation":[{"name":"Internet Medical Center, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine)","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linhan","family":"Zhong","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine)","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Geriatrics, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine)","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Geriatrics, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine)","place":["Hangzhou, Zhejiang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,22]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.Cd-23-1266","article-title":"Il2 targeted to cd8+ t cells promotes robust effector t-cell responses and potent antitumor immunity","volume":"14","author":"Moynihan","year":"2024","journal-title":"Cancer Discov"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1158\/2159-8290.Cd-24-1232","article-title":"Tumor-associated nk cells regulate distinct cd8+ t-cell differentiation program in cancer and contribute to resistance against immune checkpoint blockers","volume":"15","author":"Song","year":"2025","journal-title":"Cancer Discov"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2019.01719","article-title":"T cell dysfunction in cancer immunity and 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