Literature DB >> 3264356

Transfer of experimental glomerulonephritis in chickens by mononuclear cells.

W K Bolton1, M Chandra, T M Tyson, P R Kirkpatrick, M J Sadovnic, B C Sturgill.   

Abstract

We have produced experimental autoimmune glomerulonephritis (EAG) in histocompatible SC chickens by immunization with different types of glomerular antigen. The development of EAG was time, but not antigen, dependent. Transfer of mononuclear cells from spleens and kidneys of nephritic animals resulted in EAG in naive recipients. Transferred EAG developed earlier than in immunized donors and was not associated with circulating or bound anti-GBM antibodies. Control recipients did not develop disease from control cells alone, soluble antigen, or antigen plus control cells. The cells which transferred EAG appeared morphologically by light and electron microscopy to be lymphocytes, sedimented as lymphocytes, were positive with anti-serum to thymocytes but negative with anti-bursa anti-serum, stained as T-cells with monoclonal antibodies and underwent blast transformation in response to mitogen and GBM antigen. Other organ specific diseases have been transferred by cells alone; to our knowledge this is the first description of glomerulonephritis transferred by cells alone. This new pathogenetic process may play an important role in the development of glomerulonephritis in other animal models as well as in humans.

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Year:  1988        PMID: 3264356     DOI: 10.1038/ki.1988.224

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  11 in total

1.  What sensitized cells just might be doing in glomerulonephritis.

Authors:  W Kline Bolton
Journal:  J Clin Invest       Date:  2002-03       Impact factor: 14.808

Review 2.  Basement membranes and autoimmune diseases.

Authors:  Mary H Foster
Journal:  Matrix Biol       Date:  2016-08-02       Impact factor: 11.583

Review 3.  Update on crescentic glomerulonephritis.

Authors:  Carole Hénique; Christina Papista; Léa Guyonnet; Olivia Lenoir; Pierre-Louis Tharaux
Journal:  Semin Immunopathol       Date:  2014-06-20       Impact factor: 9.623

Review 4.  T cell subsets in glomerular diseases.

Authors:  S Florquin; M Goldman
Journal:  Springer Semin Immunopathol       Date:  1994

5.  IL-23, not IL-12, directs autoimmunity to the Goodpasture antigen.

Authors:  Joshua D Ooi; Richard K S Phoon; Stephen R Holdsworth; A Richard Kitching
Journal:  J Am Soc Nephrol       Date:  2009-04-08       Impact factor: 10.121

6.  Kidney dendritic cell activation is required for progression of renal disease in a mouse model of glomerular injury.

Authors:  Felix Heymann; Catherine Meyer-Schwesinger; Emma E Hamilton-Williams; Linda Hammerich; Ulf Panzer; Sylvia Kaden; Susan E Quaggin; Jürgen Floege; Hermann-Josef Gröne; Christian Kurts
Journal:  J Clin Invest       Date:  2009-04-20       Impact factor: 14.808

Review 7.  New insights into mechanisms of immune glomerular injury.

Authors:  W G Couser
Journal:  West J Med       Date:  1994-05

Review 8.  The inflammatory function of renal glomerular mesangial cells and their interaction with the cellular immune system.

Authors:  H H Radeke; K Resch
Journal:  Clin Investig       Date:  1992-09

9.  Th1 and Th17 cells induce proliferative glomerulonephritis.

Authors:  Shaun A Summers; Oliver M Steinmetz; Ming Li; Joshua Y Kausman; Timothy Semple; Kristy L Edgtton; Dorin-Bogdan Borza; Hal Braley; Stephen R Holdsworth; A Richard Kitching
Journal:  J Am Soc Nephrol       Date:  2009-10-09       Impact factor: 10.121

10.  Molecular mapping of the Goodpasture's epitope for glomerulonephritis.

Authors:  W Kline Bolton; Lanlin Chen; Thomas Hellmark; Jay Fox; Jorgen Wieslander
Journal:  Trans Am Clin Climatol Assoc       Date:  2005
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