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Acute blockade or genetic deletion of CLIC1 markedly attenuates microglial surveillance by reducing ramification and motility, without affecting chemotaxis. This phenotype is recapitulated in xenografted human microglia and human brain tissue. Mechanistically, CLIC1 effects involve interactions with actin-binding ezrin, radixin, and moesin (ERM) proteins, suggesting a role in linking the plasma membrane to the cytoskeleton. Contrary to its name, CLIC1 functions are chloride-independent and thus unlikely to reflect ion channel activity. This is supported by patch-clamp electrophysiology revealing lack of chloride conductance in surveillant microglia. Following ATP\u2013evoked activation, CLIC1 blockade strongly suppresses NLRP3\u2013dependent interleukin-1\u03b2 release, suggesting therapeutic potential against neuroinflammation.<\/jats:p>","DOI":"10.1126\/sciadv.ads9181","type":"journal-article","created":{"date-parts":[[2025,10,22]],"date-time":"2025-10-22T17:59:42Z","timestamp":1761155982000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":7,"title":["The chloride intracellular channel 1 (CLIC1) is essential for microglial morphodynamics and neuroinflammation"],"prefix":"10.1126","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5801-4358","authenticated-orcid":true,"given":"Ali","family":"Rifat","sequence":"first","affiliation":[{"name":"Institute of Neurophysiology, Charit\u00e9 - Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin and Humboldt-Universit\u00e4t zu Berlin, Charit\u00e9platz 1, 10117 Berlin, Germany."},{"name":"Berlin Institute of Health at Charit\u00e9 - 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