rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
|
pubmed:dateCreated |
2001-5-23
|
pubmed:abstractText |
Mice with a targeted disruption of the gene encoding a lymphoid-expressed orphan G protein-coupled receptor, G2A, demonstrate a normal pattern of T and B lineage differentiation through young adulthood. As G2A-deficient animals age, they develop secondary lymphoid organ enlargement associated with abnormal expansion of both T and B lymphocytes. Older G2A-deficient mice (>1 year) develop a slowly progressive wasting syndrome, characterized by lymphocytic infiltration into various tissues, glomerular immune complex deposition, and anti-nuclear autoantibodies. G2A-deficient T cells are hyperresponsive to TCR stimulation, exhibiting enhanced proliferation and a lower threshold for activation. Our findings demonstrate that G2A plays a critical role in controlling peripheral lymphocyte homeostasis and that its ablation results in the development of a novel, late-onset autoimmune syndrome.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
1074-7613
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
14
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
561-71
|
pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11371358-Animals,
pubmed-meshheading:11371358-Autoimmune Diseases,
pubmed-meshheading:11371358-Autoimmunity,
pubmed-meshheading:11371358-B-Lymphocytes,
pubmed-meshheading:11371358-Cell Cycle Proteins,
pubmed-meshheading:11371358-Cell Division,
pubmed-meshheading:11371358-Female,
pubmed-meshheading:11371358-GTP-Binding Proteins,
pubmed-meshheading:11371358-Lymph Nodes,
pubmed-meshheading:11371358-Male,
pubmed-meshheading:11371358-Mice,
pubmed-meshheading:11371358-Mice, Inbred BALB C,
pubmed-meshheading:11371358-Mice, Inbred C57BL,
pubmed-meshheading:11371358-Mice, Knockout,
pubmed-meshheading:11371358-Receptors, Antigen, T-Cell,
pubmed-meshheading:11371358-Receptors, Cell Surface,
pubmed-meshheading:11371358-Receptors, G-Protein-Coupled,
pubmed-meshheading:11371358-T-Lymphocytes,
pubmed-meshheading:11371358-Time Factors
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pubmed:year |
2001
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pubmed:articleTitle |
Mice lacking the orphan G protein-coupled receptor G2A develop a late-onset autoimmune syndrome.
|
pubmed:affiliation |
Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|