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Nasal administration of an anti-CD3 monoclonal antibody (aCD3 mAb) has shown therapeutic benefits in autoimmune and CNS disease models. Using a respiratory-restricted mild SARS-CoV-2 mouse model of Long COVID, we show that nasal anti-CD3 mAb, administered shortly after infection or during chronic neuroinflammation, increased brain FoxP3+ IL\u201310+ Tregs, reduced microglial and astrocytic gliosis in the white matter and hippocampus, restored neurogenesis, and improved short-term memory. Nasal aCD3 mAb reprogrammed microglia from an antigen-presenting, NF-\u03baB-driven inflammatory state toward chemokine signaling, phagosome, and TGF \u03b2\u2013related regulatory phenotype. Patients with Long COVID with neurological symptoms had lower circulating Treg populations. These findings identify nasal administration of aCD3 mAb as a noninvasive strategy to control neuroinflammation, restore the neurogenic niche, and offer a novel approach to treating cognitive impairment in Long COVID.<\/jats:p>","DOI":"10.64898\/2026.04.07.716934","type":"posted-content","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T03:50:11Z","timestamp":1775706611000},"source":"Crossref","is-referenced-by-count":0,"title":["Intranasal Anti-CD3 Antibody Treatment Attenuates Post\u2013COVID Neuroinflammation and Enhances Hippocampal Neurogenesis and Cognitive Function in Mice"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6118-872X","authenticated-orcid":false,"given":"Peiwen","family":"Lu","sequence":"first","affiliation":[{"name":"Department of Immunobiology, Yale University, New Haven CT 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