Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
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
pubmed:year
2001
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.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't