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  • Title: Evidence for an intrinsic B cell defect in lpr/lpr mice apparent in neonatal chimeras.
    Author: Perkins DL, Glaser RM, Mahon CA, Michaelson J, Marshak-Rothstein A.
    Journal: J Immunol; 1990 Jul 15; 145(2):549-55. PubMed ID: 2365994.
    Abstract:
    Stem cells from a lpr/lpr mouse do not cause the lpr syndrome characteristic of unmanipulated MRL/lpr mice when injected into nonautoimmune neonatal mice. Instead, these neonatal chimeras gradually become markedly lymphopenic. As adults, only limited donor cell engraftment (approximately 5%) was evident as assessed by cell surface staining of H-2D or Thy-1 allelic markers. However, the relatively low number of lpr/lpr-derived B cells produced greater than 90% of the circulating IgG2a antibody and all detectable IgG2a anti-ssDNA autoantibody, indicating that lpr/lpr B cells express an intrinsic genetic defect resulting in hyper-IgG and autoantibody secretion.
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