Αlpha¹ Record ID: F78DB17A
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Lu, P.; Izzy, S.; Da Silva, P.; Imkamp, H. T.; Christenson, J. R.; Yahya, T.; Mansi, M. H. A.; Alawi, A.; Moreira, T. G.; Monje et al.
Cognitive impairment is a disabling feature of Long COVID, with data supporting neuroinflammation and maladaptive glial responses as primary drivers. 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-10+ 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-{kappa}B-driven inflammatory state toward chemokine signaling, phagosome, and TGF {beta}-related 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.
In a mouse model of Long COVID brain fog, a nasal squirt of anti-CD3 antibody acts like an immune reset button—even weeks after infection. It dampens cranky microglia, boosts neuron birth in the hippocampus, and sharpens memory.
Shared by immunologist Prof. Akiko Iwasaki (@VirusesImmunity) as lead senior author. Generated buzz among Long COVID researchers for its therapeutic potential. Praised for the elegant mouse model and timely implications
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