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 language | English (US) |
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Article number | 143 |
Pages (from-to) | 561-571 |
Number of pages | 11 |
Journal | Immunity |
Volume | 14 |
Issue number | 5 |
DOIs | |
State | Published - 2001 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Infectious Diseases