Autoimmune Disease Strongly Resembling Systemic Lupus Erythematosus (SLE) in F1 Mice Undergoing Graft-Versus-Host Reaction (GVHR)

  • F. M. van der Veen
  • A. G. Rolink
  • E. Gleichmann
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 149)


The etiology and cellular pathogenesis of human SLE and of the spontaneously arising SLE-like diseases of mice are still poorly understood. Especially, the possible participation of T helper (TH) cells and, if this exists, the mode of action by which it causes the formation of multiple IgG autoantibodies is unclear (1). There is general agreement, however, that in both SLE and SLE-like conditions there is a B-cell hyperactivity (1), which has sometimes been referred to as “polyclonal” B-cell stimulation (2). Since potentially autoreactive B cells exist in normal individuals (3), they might be switched on to antibody production in states of generalized B-cell hyperactivity. Indeed, it has been possible to induce the formation of various SLE-like autoantibodies in nonautoimmune strains of mice by the administration of the polyclonal B-cell activator lipopolysaccharide (LPS) (4,5). However, there are no reports which indicate that LPS can induce the severe clinical and pathological alterations characteristic of SLE. Moreover, there is no evidence suggesting that human SLE patients are exposed to an abnormal load of bacterial products capable of inducing polyclonal B-cell stimulation.


Systemic Lupus ERYTHEMATOSUS Nuclear Antigen Optimal Induction Human Systemic Lupus ERYTHEMATOSUS Cellular Pathogenesis 
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Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • F. M. van der Veen
    • 1
  • A. G. Rolink
    • 1
  • E. Gleichmann
    • 1
  1. 1.Central Laboratory of the Netherlands Red Cross Blood, Transfusion Service and Laboratory of Experimental and Clinical ImmunologyUniversity of AmsterdamAmsterdamThe Netherlands

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