Abstract:
:The investigations with the NZB X SWR model show that the development of systemic autoimmune disease is a multistep, multigene process. Severe lupus nephritis in the NZB X SWR hybrids results from the interaction of genes inherited from both the autoimmune NZB and the normal SWR parents. A similar genetic interaction occurs in the NZB X NZW hybrids, but in this model, both the parental strains are abnormal and the nature of the gene products or their mechanism of action is unknown. In the NZB X SWR model, we have been able to identify a restricted subpopulation of nephritogenic anti-DNA antibody idiotypes that are encoded by genes of the normal SWR parents. Thus, these are one set of genes that determine the development of severe lupus nephritis in the F1 hybrids. In addition, another set of genes allows for the expansion of B cells that produce such pathogenic anti-DNA idiotypes in the F1 hybrids since such B-cell clones remain dormant in the normal SWR parents. The latter category of genes, presumably specifying defects in immunoregulation, are probably inherited from the NZB parents or may be the result of complementation of genes inherited from both parents. Further investigations with the NZB X SWR model will help us define the immunoregulatory defects in SLE that are specific for the T and B cells involved in pathogenic autoantibody production.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Datta SK,Gavalchin Jdoi
10.1111/j.1749-6632.1986.tb20855.xsubject
Has Abstractpub_date
1986-01-01 00:00:00pages
47-58eissn
0077-8923issn
1749-6632journal_volume
475pub_type
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
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journal_title:Annals of the New York Academy of Sciences
pub_type: 杂志文章
doi:10.1111/j.1749-6632.1976.tb47694.x
更新日期:1976-01-01 00:00:00