Linked Life Data

19935804

Source:http://linkedlifedata.com/resource/pubmed/id/19935804

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2009-11-25
pubmed:abstractText
In germinal centres, somatic hypermutation and B cell selection increase antibody affinity and specificity for the immunizing antigen, but the generation of autoreactive B cells is an inevitable by-product of this process. Here, we review the evidence that aberrant selection of these autoreactive B cells can arise from abnormalities in each of the germinal centre cellular constituents--B cells, T follicular helper cells, follicular dendritic cells and tingible body macrophages--or in the supply of antigen. As the progeny of germinal centre B cells includes long-lived plasma cells, selection of autoreactive B cells can propagate long-lived autoantibody responses and cause autoimmune diseases. Elucidation of crucial molecular signals in germinal centres has led to the identification of novel therapeutic targets.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1474-1741
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
845-57
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Dysregulation of germinal centres in autoimmune disease.
pubmed:affiliation
John Curtin School of Medical Research, Australian National University, GPO Box 334, Canberra, ACT 2601, Australia. carola.vinuesa@anu.edu.au
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't