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- W3022920667 abstract "Abstract Lymphocyte depletion using anti‐CD52 antibody effectively reduces relapses of multiple sclerosis (MS). To begin to understand what mechanisms might control this outcome, we examined the effect of a murine‐CD52‐specific mAb on the depletion and repopulation of immune cells in mice with experimental autoimmune encephalomyelitis (EAE), a model of MS. We tested whether the tolerance‐promoting receptor programmed cell death protein‐1 (PD‐1) is required for disease remission post anti‐CD52, and found that PD‐1‐deficient mice with a more severe EAE were nevertheless effectively treated with anti‐CD52. Anti‐CD52 increased the proportions of newly generated T cells and double‐negative (DN) T cells while reducing newly generated B cells; the latter effect being associated with a higher expression of CD52 by these cells. In the longer term, anti‐CD52 caused substantial increases in the proportion of newly generated lymphocytes and DN T cells in mice with EAE. Thus, the rapid repopulation of lymphocytes from central lymphoid organs post anti‐CD52 may limit further disease. Furthermore, these data identify DN T cells, a subset with immunoregulatory potential, as a significant hyperrepopulating subset following CD52‐mediated depletion." @default.
- W3022920667 created "2020-05-13" @default.
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- W3022920667 creator A5074812414 @default.
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- W3022920667 date "2020-05-27" @default.
- W3022920667 modified "2023-09-27" @default.
- W3022920667 title "Anti‐CD52 blocks EAE independent of PD‐1 signals and promotes repopulation dominated by double‐negative T cells and newly generated T and B cells" @default.
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- W3022920667 doi "https://doi.org/10.1002/eji.201948288" @default.
- W3022920667 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32388861" @default.
- W3022920667 hasPublicationYear "2020" @default.
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