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- W4313383337 abstract "Abstract The pathogenesis of neuropsychiatric systemic lupus erythematosus (NPSLE) remains unclear, despite the large number of lupus patients affected by neuropsychiatric manifestations. We recently showed that MRL/lpr mice, a classic SLE mouse model with neuropsychiatric symptoms, develop tertiary lymphoid structures (TLS) (a.k.a. ectopic germinal centers). TLS structurally and functionally resemble lymph nodes and form at the site of chronic inflammation to create more localized and specialized immune responses, which may promote a local immune response against self-antigen and thus contribute to the pathogenesis. Since CXCL13 is a key chemokine that drives lymphoid formation, we injected female MRL/lpr mice intraperitoneally with an anti-CXCL13 antibody, an IgG isotype control antibody, or PBS three times weekly for 12 weeks starting at 6–8 weeks of age. Cognitive dysfunction and affective deficits were assessed at the end of treatment. Anti-CXCL13 mAb treated MRL/lpr mice showed significant improvement in spatial memory, recognition memory, and depression-like behavior as compared to the two control groups (p=0.034, p=0.013, and p=0.0087, respectively). Furthermore, mice receiving the antibody by intracerebroventricular delivery showed similar results (p=0.055, p=0.20, and p=0.018, respectively). There were, however, no apparent differences in indicators of systemic disease, including autoantibody titers. Our results suggest that TLS play an important role in the pathophysiology of affective deficits and cognitive dysfunction, and that CXCL13 neutralization may be a potential therapeutic strategy to target NPSLE." @default.
- W4313383337 created "2023-01-06" @default.
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- W4313383337 date "2020-05-01" @default.
- W4313383337 modified "2023-09-27" @default.
- W4313383337 title "Neutralizing CXCL13 attenuates neuropsychiatric manifestations in lupus-prone mice" @default.
- W4313383337 doi "https://doi.org/10.4049/jimmunol.204.supp.236.8" @default.
- W4313383337 hasPublicationYear "2020" @default.
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