Linked Life Data

15084263

Source:http://linkedlifedata.com/resource/pubmed/id/15084263

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-4-15
pubmed:abstractText
During illness and stress, the immune system can suffer a considerable loss of T cells (lymphopenia). The remaining T cells undergo vigorous compensatory expansion, known as homeostatic proliferation, to reconstitute the immune system. Interestingly, human diseases of autoimmune etiology often present with immune deficiencies such as lymphopenia. In this study, we show that reduced T cell numbers and the resulting exaggerated homeostatic-type proliferation of T cells generate autoimmunity. The cycling T cell population is short lived, and the depleted memory compartment fuels the generation of new effector T cells. A catalyst for these phenomena is the increased responses to the cytokine IL-21, a mediator that regulates T cell turnover. We conclude that poor T cell survival and lymphopenia precipitate autoimmune disease.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
265-77
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Homeostatic expansion of T cells during immune insufficiency generates autoimmunity.
pubmed:affiliation
Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't