Linked Life Data

1574128

Source:http://linkedlifedata.com/resource/pubmed/id/1574128

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6373
pubmed:dateCreated
1992-6-1
pubmed:abstractText
Studies on transgenic mice expressing immunoglobulins against self-antigens have shown that self-tolerance is maintained by active elimination (clonal deletion), functional inactivation (clonal anergy) of self-reactive B cells, or a combination of both. We have established and characterized a transgenic mouse line expressing an anti-erythrocyte autoantibody. In contrast to other autoantibody transgenic lines, about 50% of the animals of this transgenic line suffer from autoimmune disease, indicating a loss of self-tolerance. Here we show that peritoneal Ly-1 B cells (also known as B-1 cells) are responsible for this autoimmune disease in our transgenic mice. A few self-reactive Ly-1 B cells that have somehow escaped the deletion mechanism expand in the peritoneum because of the absence of self-antigen. These Ly-1 B cells are eliminated in vivo by apoptosis once exposed to self-antigen. On the basis of these results we propose a novel autoantibody production mechanism whereby self-reactive B cells sequestered in compartments free of self-antigens may survive, proliferate and be activated for generation of pathogenic autoantibodies in autoimmune diseases.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
357
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
77-80
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Antigen-induced apoptotic death of Ly-1 B cells responsible for autoimmune disease in transgenic mice.
pubmed:affiliation
Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't