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

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Affiliations

  • 1. Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, Los Angeles, CA 90095, USA.
      Authors
    • Le LQ 1
    (1 author)

ORCIDs linked to this article

Immunity, 01 May 2001, 14(5):561-571
https://doi.org/10.1016/s1074-7613(01)00145-5 PMID: 11371358 

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.

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Read article at publisher's site: https://doi.org/10.1016/s1074-7613(01)00145-5

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NCI NIH HHS (2)