{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T01:42:07Z","timestamp":1792978927570,"version":"4.5.0"},"reference-count":72,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T00:00:00Z","timestamp":1770854400000},"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>Prostate cancer (PCa) has long been viewed as an immunologically \u201ccold\u201d malignancy because immune checkpoint inhibitors (ICIs) show limited benefit in unselected patients, particularly after progression to metastatic castration-resistant PCa (mCRPC) or treatment-related neuroendocrine PCa (NEPC). Single-cell and spatial profiling now reveal immune heterogeneity across patients, between lesions, and along the path from localized disease to metastasis. Primary tumors form mosaics of immune-excluded glands, myeloid-suppressed stromal borders, and focal lymphocyte-rich niches with B-cell aggregates and tertiary lymphoid structures (TLS). TLS-high regions represent an actionable \u201chot minority\u201d resembling inflamed, ICI-responsive cancers, supporting biomarker-guided neoadjuvant or focal immunotherapy. With dissemination, heterogeneity expands across sites; bone metastases become marrow immune organs dominated by suppressive macrophage\/monocyte programs and dysfunctional T cells, often driven by the CCL2\u2013CCR6 axis. Standard therapies remodel these ecosystems, creating inflammatory windows yet fostering adaptive resistance. Mechanistically, myeloid-driven, inflammation-coupled rewiring is central to escape: IL-8\/CXCR2 signaling and therapy-induced senescence\/SASP recruit and polarize suppressive myeloid cells, reinforcing T-cell exclusion and exhaustion. Variable HLA class I loss and hypoxic or metabolic \u201cfunctional cold zones\u201d add lesion-specific immune invisibility. Clinically, these insights motivate a heterogeneity-aware framework integrating genomic responder subsets with microenvironmental stratification. Barrier-matched strategies include T-cell redirection (PSMA\/STEAP1 engagers, bispecifics, CAR-T) and combinations that heat or modulate myeloid cells. Treating immune heterogeneity as a clinical variable enables durable immunotherapy in PCa.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1753718","type":"journal-article","created":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T06:50:56Z","timestamp":1770879056000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["Clinically oriented immune heterogeneity in prostate cancer: emerging targets and strategies"],"prefix":"10.3389","volume":"17","author":[{"given":"MingWei","family":"Zhan","sequence":"first","affiliation":[{"name":"Department of Urology, Hangzhou TCM Hospital of Zhejiang Chinese Medical University (Hangzhou Hospital of Traditional Chinese Medicine)","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"BinBin","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Urology, Hangzhou TCM Hospital of Zhejiang Chinese Medical University (Hangzhou 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