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

L. Q. Le, J. H S Kabarowski, Z. Weng, A. B. Satterthwaite, E. T. Harvill, E. R. Jensen, J. F. Miller, O. N. Witte

Research output: Contribution to journalArticle

154 Scopus citations


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)
Pages (from-to)561-571
Number of pages11
Issue number5
Publication statusPublished - 2001


ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology

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