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We show here that an innate immune, cytokine response after tubule injury is required and sufficient to induce adult zebrafish kidney regeneration. An injury reporter zebrafish transgenic,\n                  <jats:italic>Tg(kim1:mScarlet3),<\/jats:italic>\n                  revealed that tubule injury occurred specifically in kidney proximal tubules and was associated with a rapid accumulation of neutrophils and macrophages. Injury also activated a\n                  <jats:italic>Tg(NFkB:GFP)<\/jats:italic>\n                  reporter transgene specifically in kidney tubules where RNA seq revealed NFkB target gene and cytokine expression. Inhibition of NFkB signaling with JSH-23 blocked\n                  <jats:italic>Tg(NFkB:GFP)<\/jats:italic>\n                  reporter activation and also inhibited induction of new nephrons. Systemic injection of the immune activators lipopolysaccharide or zymosan into uninjured fish rapidly induced cytokine expression followed by nephrogenic gene expression and the appearance of new, functional nephrons. Analysis of injury-induced cytokines revealed that several paralogs of\n                  <jats:italic>cxcl11<\/jats:italic>\n                  were strongly expressed throughout the regeneration response and injection of recombinant Cxcl11 was sufficient to induce FGF-dependent kidney stem cell aggregation, but not Wnt-dependent epithelial differentiation. Kidney injury in zebrafish expressing a neutrophil dominant negative\n                  <jats:italic>rac2D57N<\/jats:italic>\n                  transgene activated Fgf signaling but failed to induce\n                  <jats:italic>wnt9b<\/jats:italic>\n                  or downstream Wnt target genes. Nephrogenic gene expression and epithelial tubule formation was rescued by treatment with the canonical Wnt agonist CHIR. Our findings demonstrate that an injury-induced, sterile immune response regulates kidney regeneration by establishing a nephrogenic niche of Fgf and Wnt signaling that supports tissue-resident kidney stem cell differentiation into functional nephrons.\n                <\/jats:p>","DOI":"10.64898\/2026.04.08.717325","type":"posted-content","created":{"date-parts":[[2026,4,11]],"date-time":"2026-04-11T04:55:15Z","timestamp":1775883315000},"source":"Crossref","is-referenced-by-count":0,"title":["Injury-induced Cxcl11 and neutrophil signaling drive zebrafish kidney regeneration by generating a nephrogenic niche of Fgf and Wnt expression"],"prefix":"10.64898","author":[{"given":"Olaleye","family":"Olajuyin","sequence":"first","affiliation":[{"name":"Davis Center for Regenerative Biology and Aging, Mount Desert Island Biological Laboratory, Bar Harbor ME 04605"},{"name":"Graduate School of Biomedical Science and Engineering, University of Maine, Orono ME 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