| First Author | Ma N | Year | 2015 |
| Journal | Clin Immunol | Volume | 160 |
| Issue | 2 | Pages | 142-54 |
| PubMed ID | 26071318 | Mgi Jnum | J:308048 |
| Mgi Id | MGI:6727857 | Doi | 10.1016/j.clim.2015.05.016 |
| Citation | Ma N, et al. (2015) Ligation of metabotropic glutamate receptor 3 (Grm3) ameliorates lupus-like disease by reducing B cells. Clin Immunol 160(2):142-54 |
| abstractText | Recently B-cell activating factor (BAFF) was identified by our group and others as a novel therapeutic target for the treatment of autoimmune diseases. To expand upon this, we utilized microarrays to screen for molecules upregulated in B cells from BAFF-inhibited mice with lupus-like disease and identified metabotropic glutamate receptor 3 (Grm3). In addition to confirming the expression of this receptor in B cells, a synthetic agonist of Grm3 was found to downregulate B cells and ameliorate autoimmune symptoms in mice. Conversely, a Grm3 antagonist increased B-cell numbers and further aggravated disease. Thus, these results suggest that activation of Grm3 ameliorates lupus-like disease in mice by reducing B cell numbers. Not only do the findings presented in this study increase our understanding of the inhibitory signals initiated on the surface of B cells, but they also identify a novel potential target for the treatment of autoimmune diseases. |
