| First Author | Feng BS | Year | 2018 |
| Journal | Arch Biochem Biophys | Volume | 657 |
| Pages | 8-14 | PubMed ID | 30217509 |
| Mgi Jnum | J:266972 | Mgi Id | MGI:6237104 |
| Doi | 10.1016/j.abb.2018.09.003 | Citation | Feng BS, et al. (2018) Bcl2L12 mediates effects of protease-activated receptor-2 on the pathogenesis of Th2-dominated responses of patients with ulcerative colitis. Arch Biochem Biophys 657:8-14 |
| abstractText | The immune dysregulation plays an important role in the pathogenesis of ulcerative colitis (UC). Bcl2 like protein-12 (Bcl2L12) and mast cells are involved in immune dysregulation of UC. This study aims to elucidate the role of Bcl2L12 in the contribution to the pathogenesis of T helper (Th)2-biased inflammation in UC patients. The results showed that Bcl2L12 was expressed by peripheral CD4(+) T cells that was associated with Th2 polarization in UC patients. Bcl2L12 mediated the protease-activated receptor-2 (PAR2)-induced IL-4 expression in CD4(+) cells. Activation of PAR2 increased expression of Bcl2L12 in CD4(+) T cells. Bcl2L12 mRNA decayed spontaneously in CD4(+) T cells after separated from UC patients which was prevented by activating PAR2. Bcl2L12 mediated the binding between GATA3 and the Il4 promoter in CD4(+) T cells. Mice with Bcl2L12 deficiency failed to induce Th2-biased inflammation in the colon mucosa. We conclude that CD4(+) T cells from UC patients expressed high levels of Bcl2L12; the latter plays an important role in the development of Th2-biased inflammation in the intestine. Bcl2L12 may be a novel therapeutic target in the treatment of Th2-biased inflammation. |
