| First Author | Le LQ | Year | 2001 |
| Journal | Immunity | Volume | 14 |
| Issue | 5 | Pages | 561-71 |
| PubMed ID | 11371358 | Mgi Jnum | J:69473 |
| Mgi Id | MGI:1934708 | Doi | 10.1016/s1074-7613(01)00145-5 |
| Citation | Le LQ, et al. (2001) Mice lacking the orphan G protein-coupled receptor G2A develop a late-onset autoimmune syndrome. Immunity 14(5):561-71 |
| 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. |
