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Life sciences · Journal article
Cancer Immunology Immunotherapy · October 2, 2026
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Abstract Regulatory B cells (Bregs) restrain effector immunity through interleukin-10 (IL-10), IL-35, and transforming growth factor beta (TGF-β), and their induction depends on signals supplied by the host microbiota. Two mechanistic axes anchor this relationship. Gut commensals drive myeloid IL-1β and IL-6 production, which acts on B cell IL-1 and IL-6 receptors to generate IL-10-competent Bregs in spleen and mesenteric lymph nodes. Microbially derived short-chain fatty acids, principally butyrate, amplify aryl hydrocarbon receptor signalling in Bregs and increase suppressive capacity rather than Breg number. Both axes matter for checkpoint blockade because the IL-10 programme that limits immune-related adverse events (irAEs) also suppresses tumour-directed CD8 responses. We use the gut lung axis as the framework linking intestinal microbial ecology to thoracic tumour immunology, and we separate cancer-derived evidence from data generated in autoimmune and inflammatory models. Four gaps are testable: whether gut-induced Bregs traffic to the lung tumour microenvironment or its draining lymph nodes; whether lung commensals generate lung-resident Bregs as pancreatic commensals do through epithelial IL-1β; whether microbiota-selected B cell receptor clonotypes feed the Breg pool; and which metabolic programme sustains human Bregs in tumours. Healthy-donor faecal microbiota transplantation (FMT) before checkpoint blockade produced objective response rates of 80% in first-line non-small cell lung cancer and 75% in melanoma, and the live biotherapeutic CBM588 added to nivolumab and ipilimumab in renal cell carcinoma gave a progression-free survival hazard ratio of 0.15 (95% CI 0.05–0.47). Risk is specific: donor screening excludes most candidates, drug-resistant Escherichia coli bacteraemia has followed FMT, and transmission of procarcinogenic bacteria remains possible.