{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T06:01:58Z","timestamp":1785132118901,"version":"3.55.0"},"reference-count":110,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T00:00:00Z","timestamp":1785110400000},"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:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Immune escape remains a major barrier to durable benefit from immunotherapy in breast cancer, particularly in immune-cold tumors and those with an immune-excluded architecture. Emerging evidence from cancer neuroscience suggests that nerves are not passive bystanders of the tumor microenvironment, but active regulators of stromal remodeling, myeloid polarization, T-cell dysfunction, metastatic adaptation, and neuroendocrine stress biology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main body<\/jats:title>\n                    <jats:p>We synthesize current evidence supporting a multiscale model of neuro\u2013immune crosstalk in breast cancer. We first examine sympathetic innervation as an upstream coordinator of immunosuppressive signaling through \u03b2-adrenergic pathways that reshape myeloid compartments, lymphangiogenesis, and effector lymphocyte fitness. We then discuss sensory-nerve-driven immune exclusion, focusing on CGRP\u2013CAF\u2013ECM circuits and Substance P-associated inflammatory relays that stabilize prometastatic states. Next, we review direct nerve\u2013tumor interfaces, including neurotransmitter-dependent synapse-like signaling, pseudo-synaptic coupling, extracellular-vesicle\/TNT-mediated metabolic communication, and mitochondrial transfer, and evaluate their potential roles in immune resistance and metastatic competence. We further integrate these local interactions into a systems framework by considering tumor\u2013brain\u2013sympathetic feedback loops and neuroendocrine outputs that reset host immune thresholds while emphasizing the context-dependent nature of neural regulation across tumor types and microenvironmental states. Finally, we summarize neurodevelopmental programs co-opted during metastasis, discuss emerging technologies for neural phenotyping and spatial analysis, and highlight clinically actionable vulnerabilities, including \u03b2-blockade, CGRP-axis modulation, RET\/TRK-targeted therapy, and phenotype-guided combination strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This framework positions neural signaling as an upstream integrator of immune escape in breast cancer and suggests that neural biology may enable biologically informed stratification of immunotherapy-resistant tumors into distinct and targetable states.<\/jats:p>\n                  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