کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6087205 | 1589428 | 2015 | 13 صفحه PDF | دانلود رایگان |
- Blockade of BAFF upregulated Grm3 expression in B cells of lupus-like mice.
- Grm3 expression was reduced in B cells from autoimmune diseases.
- Grm3 agonist downregulated B-cell numbers and ameliorate lupus symptoms in mice.
- Grm3 antagonist increased B-cell numbers and further aggravated the disease.
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.
Journal: Clinical Immunology - Volume 160, Issue 2, October 2015, Pages 142-154