Mice lacking the orphan G protein-coupled receptor G2A develop a late-onset autoimmune syndrome

Lu Q. Le, Janusz H.S. Kabarowski, Zhigang Weng, Anne B. Satterthwaite, Eric T. Harvill, Eric R. Jensen, Jeff F. Miller, Owen N. Witte

Research output: Contribution to journalArticlepeer-review

166 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article number143
Pages (from-to)561-571
Number of pages11
JournalImmunity
Volume14
Issue number5
DOIs
StatePublished - 2001

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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