Evidence for an intrinsic B cell defect in lpr/lpr mice apparent in neonatal chimeras.
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.
Perkins
D L
DL
Department of Microbiology, Boston University School of Medicine, MA 02118.
Glaser
R M
RM
Mahon
C A
CA
Michaelson
J
J
Marshak-Rothstein
A
A
D000818:Animals; D000831:Animals, Newborn; D001323:Autoantibodies / Q000032:analysis; D001402:B-Lymphocytes / Q000276:immunology*; D016026:Bone Marrow Transplantation / Q000276:immunology; D006086:Graft vs Host Disease / Q000276:immunology; D007126:Immunoglobulin Allotypes; D007074:Immunoglobulin G / Q000032:analysis; D007075:Immunoglobulin M / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D051379:Mice; D008817:Mice, Mutant Strains; D011828:Radiation Chimera
D001323:Autoantibodies; D007126:Immunoglobulin Allotypes; D007074:Immunoglobulin G; D007075:Immunoglobulin M