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Using CRISPR\/Cas9-mediated gene deletion, we show that loss of FOLR2 severely impaired caspase-1 activation, gasdermin D cleavage, and IL-1\u03b2 release in response to multiple NLRP3 stimuli, without altering pro-IL-1\u03b2 induction. These defects were not rescued by exogenous folate and were independent of extracellular folate concentrations. Mechanistically, FOLR2\/FR\u03b2 appears to potentiate potassium efflux and the expression of multiple potassium channel\u2013encoding genes. Single-cell RNA sequencing revealed broad transcriptional repression in FR\u03b2-deficient macrophages, including genes involved in inflammasome signaling and ion transport. Genome-wide methylation profiling showed increased CpG hypermethylation in FOLR2-deficient cells, consistent with reduced transcriptional activity. Our findings indicate that FR\u03b2 promotes NLRP3 activation in a folate-independent manner potentially by regulating DNA methylation, gene transcription, and K+ efflux in macrophages. These findings uncover a previously unrecognized immunoregulatory function for FR\u03b2, positioning it as a potential modulator of macrophage-driven inflammation in contexts such as host defense, autoimmunity, and tissue-specific immune responses at the tumor and maternal\u2013fetal interface.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag051","type":"journal-article","created":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T14:39:15Z","timestamp":1776263955000},"source":"Crossref","is-referenced-by-count":3,"title":["Folate receptor beta drives NLRP3 inflammasome activation and pyroptosis in macrophages independent of folate binding"],"prefix":"10.1093","volume":"215","author":[{"given":"Lisa M","family":"Rogers","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Indiana University School of Medicine , Indianapolis, IN,","place":["United 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