Literature DB >> 1730161

Background genes mediate the development of autoimmunity in (NZB x PL/J)F1 or (NZB x BIO.PL)F1 mice.

J Schiffenbauer1, L Wegrzyn, B P Croker.   

Abstract

The (NZB x NZW)F1 mouse develops a lupus-like disease including anti-double-stranded DNA antibodies and renal disease. It has been demonstrated that genes linked to the H-2 locus contributed by NZW correlate with development of this disease. We investigated whether mice with identical class II molecules but different background genes could contribute to autoimmunity when crossed with NZB. We report that two strains, PL/J and BIO.PL, when crossed to NZB, do not result in F1 with autoimmunity. Therefore, background genes present in NZW but not in PL/J or BIO.PL contribute to the development of disease.

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Year:  1992        PMID: 1730161     DOI: 10.1016/0090-1229(92)90076-z

Source DB:  PubMed          Journal:  Clin Immunol Immunopathol        ISSN: 0090-1229


  2 in total

1.  Intrinsic B cell defects in NZB and NZW mice contribute to systemic lupus erythematosus in (NZB x NZW)F1 mice.

Authors:  L Reininger; T H Winkler; C P Kalberer; M Jourdan; F Melchers; A G Rolink
Journal:  J Exp Med       Date:  1996-09-01       Impact factor: 14.307

2.  Holes in the T cell repertoire to myelin basic protein owing to the absence of the D beta 2-J beta 2 gene cluster: implications for T cell receptor recognition and autoimmunity.

Authors:  V Kumar; E Sercarz
Journal:  J Exp Med       Date:  1994-05-01       Impact factor: 14.307

  2 in total

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