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- W567745372 abstract "Abstract Neuropsychiatric disease is a common manifestation of systemic lupus erythematosus (SLE). Potential mechanisms underlying neuropsychiatric SLE (NPSLE) include thrombosis, complement deposition, brain-reactive autoantibodies, and cytokine mediated inflammation. However, it is not clear whether the neuropsychiatric manifestations of SLE are secondary to systemic disease, or a primary pathogenic process in the brain. In order to distinguish between central nervous system (CNS) and hematopoietic contributions, we generated bone marrow chimeras between lupus-prone MRL/lpr and congenic control MRL/+ mice. We monitored systemic disease progression, performed extensive behavioral testing, and analyzed brain tissue for evidence of inflammation. MRL/lpr (donor) → MRL/lpr (recipient) chimeric mice showed significantly elevated autoantibodies and marked proteinuria while MRL/+→MRL/+ and MRL/+→MRL/lpr did not, indicating abrogation of the MRL/lpr systemic disease phenotype. Surprisingly, MRL/+→MRL/lpr mice displayed a behavioral phenotype consistent with MRL/lpr→MRL/lpr mice, including depression-like behavior and increased spatial memory deficits. In contrast, MRL/+→MRL/+ mice behaved normally. Additionally, there was elevated RANTES expression, cellular infiltration, and neurodegeneration in MRL/lpr→MRL/lpr and MRL/+→MRL/lpr chimeric mice. The data presented herein indicate that the MRL/lpr CNS is sufficient to mediate NPSLE development absent significant hematopoietic contribution." @default.
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- W567745372 date "2015-05-01" @default.
- W567745372 modified "2023-09-26" @default.
- W567745372 title "Neuropsychiatric lupus occurs independently of systemic autoimmunity (BA6P.120)" @default.
- W567745372 doi "https://doi.org/10.4049/jimmunol.194.supp.114.1" @default.
- W567745372 hasPublicationYear "2015" @default.
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