Abstract:
:In the last few years, data from experiments employing transgenic models of autoimmune disease have strengthened a particular concept of autoimmunity: disease results not so much from cracks in tolerance induction systems, leading to the generation of anti-self repertoire, as from the breakdown of secondary systems that keep these cells in check. T cells with anti-self specificities are readily found in disease-free individuals but ignore target tissues. This is also the case in some transgenic models, in spite of overwhelming numbers of autoreactive cells. In other instances, local infiltration and inflammation result, but they are well tolerated for long periods of time and do not terminally destroy target tissue. We review the possible molecular and cellular mechanisms that underlie these situations, with a particular emphasis on the destruction of pancreatic beta cells in transgenic models of insulin-dependent disease.
journal_name
Proc Natl Acad Sci U S Aauthors
André I,Gonzalez A,Wang B,Katz J,Benoist C,Mathis Ddoi
10.1073/pnas.93.6.2260subject
Has Abstractpub_date
1996-03-19 00:00:00pages
2260-3issue
6eissn
0027-8424issn
1091-6490journal_volume
93pub_type
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