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Related Experiment Videos

Experimental gold-induced autoimmunity.

H Tournade1, J C Guery, R Pasquier

  • 1INSERM U28, Hôpital Broussais, Paris, France.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|January 1, 1991
PubMed
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Aurothiopropanolsulphonate (ATPS) triggers autoimmune responses and kidney disease in Brown-Norway rats, but only interstitial nephritis in Lewis rats. Strain differences influence ATPS-induced autoimmunity and B-cell activation.

Area of Science:

  • Immunology
  • Nephrology
  • Toxicology

Background:

  • The mechanisms underlying gold-induced autoimmunity and membranous glomerulopathy remain unclear.
  • Chemicals like HgCl2 and D-penicillamine induce autoimmune conditions and membranous glomerulopathy in humans, and similar autoimmune manifestations in Brown-Norway (BN) rats but not Lewis (LEW) rats.
  • These chemicals activate T-cell clones specific for self class II major histocompatibility complex molecules, potentially causing polyclonal B-cell activation.

Purpose of the Study:

  • To investigate the effects of aurothiopropanolsulphonate (ATPS) on autoimmune responses and kidney pathology in BN and LEW rat strains.
  • To determine if ATPS induces similar autoimmune manifestations and glomerulonephritis as observed with other chemicals.
  • To explore the role of self class-II-specific T-cells in ATPS-induced autoimmunity.

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Main Methods:

  • Administration of aurothiopropanolsulphonate (ATPS) to BN and LEW rats.
  • Assessment of B-cell activation, including lymphoproliferation, hyperimmunoglobulinaemia (particularly IgE), and autoantibody production.
  • Histopathological examination of kidneys to identify glomerulonephritis and interstitial nephritis.
  • Identification of self class-II-specific T-cells.

Main Results:

  • In BN rats, ATPS induced polyclonal B-cell activation, elevated IgE levels, autoantibodies, and glomerulonephritis characterized by anti-glomerular basement membrane antibody deposition and later granular deposits, sometimes leading to membranous glomerulopathy.
  • Self class-II-specific T-cells were detected in BN rats, potentially mediating the observed polyclonal B-cell activation.
  • LEW rats did not develop glomerulopathy but showed interstitial nephritis and some degree of polyclonal B-cell activation.

Conclusions:

  • ATPS can trigger distinct autoimmune responses and varying degrees of kidney pathology depending on the rat strain.
  • The findings suggest that ATPS, like other chemicals, can induce autoimmunity via T-cell activation and subsequent B-cell stimulation.
  • Strain-dependent differences in immune responses to ATPS highlight the complexity of chemical-induced autoimmunity and its potential to affect different B-cell clones.