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Induction of murine autoimmune-disease by chronic polyclonal b-cell activation

Academic Article
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Overview

authors

  • Hang, L.
  • Slack, J. H.
  • Amundson, C.
  • Izui, S.
  • Theofilopoulos, Argyrios
  • Dixon, F. J.

publication date

  • 1983

journal

  • Journal of Experimental Medicine  Journal

abstract

  • In vivo, prolonged polyclonal activation of B cells by the nonantigenic but potent mitogenic lipid A portion of lipopolysaccharide (LPS-R595) resulted in acceleration of the late life systemic lupus erythematosus disease of female MRL/n, BXSB, and NZW mice, mimicking the time, form, and histopathological features characteristic of their early life disease counterparts, i.e., MRL/l females, BXSB males, and (NZB X NZW)F1 females. Similar polyclonal B cell activation of "immunologically normal" mice has less effect and led to a limited expression of autoimmune disease. This R595-induced autoimmunity and immune complex-mediated disease seemed to be the direct result of activation of the immune system and not from other effects of endotoxin since C3H/HeJ, a strain lacking lymphocyte receptors for LPS-R595, had neither serological nor histological evidence of autoimmune disease despite identical treatment.

subject areas

  • Animals
  • Antibody-Producing Cells
  • Autoantibodies
  • Autoimmune Diseases
  • B-Lymphocytes
  • Blood Coagulation
  • Blood Urea Nitrogen
  • Chronic Disease
  • Female
  • Glomerulonephritis
  • Hemolytic Plaque Technique
  • Heparin
  • Lupus Erythematosus, Systemic
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
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Identity

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.157.3.874

PubMed ID

  • 6339669
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Additional Document Info

start page

  • 874

end page

  • 883

volume

  • 157

issue

  • 3

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