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However, the extent to which this is a bidirectional process, and whether peripheral immune cells also promote tolerance mechanisms in the CNS remains poorly defined. Here we report that helminth-induced type 2 inflammation promotes monocyte responses in the brain that are required to inhibit excessive microglial activation and host death. Mechanistically, infection-induced monocytes express YM1 that is sufficient to inhibit tumor necrosis factor production from activated microglia. Importantly, neuroprotective monocytes persist in the brain, and infected mice are protected from subsequent lipopolysaccharide-induced neuroinflammation months after infection-induced inflammation has resolved. These studies demonstrate that infiltrating monocytes promote CNS homeostasis in response to inflammation in the periphery and demonstrate that a peripheral infection can alter the immunologic landscape of the host brain.<\/jats:p>","DOI":"10.1073\/pnas.2201645119","type":"journal-article","created":{"date-parts":[[2022,9,7]],"date-time":"2022-09-07T13:38:03Z","timestamp":1662557883000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":9,"title":["Monocytes maintain central nervous system homeostasis following helminth-induced inflammation"],"prefix":"10.1073","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2617-3626","authenticated-orcid":false,"given":"Jianya","family":"Peng","sequence":"first","affiliation":[{"name":"Center for Immunity and Inflammation, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103"},{"name":"Department of Medicine, New Jersey Medical School, Rutgers, 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