| First Author | Nakamura Y | Year | 2019 |
| Journal | Inflamm Res | Volume | 68 |
| Issue | 3 | Pages | 223-230 |
| PubMed ID | 30564895 | Mgi Jnum | J:295122 |
| Mgi Id | MGI:6459664 | Doi | 10.1007/s00011-018-1207-y |
| Citation | Nakamura Y, et al. (2019) Malt1 inactivation attenuates experimental colitis through the regulation of Th17 and Th1/17 cells. Inflamm Res 68(3):223-230 |
| abstractText | OBJECTIVE AND DESIGN: Protease activity of MALT lymphoma-translocation protein 1 (Malt1) plays an important role in the development of colitis, but the detailed mechanism has not been fully elucidated. METHOD: Effects of Malt1 protease on the activation of T cells and the development of experimental colitis was investigated using Malt1 protease-deficient (PD) mouse. RESULTS: IL-2 production from CD4(+) T cells of Malt1 PD mice was decreased compared with that of wild-type (WT) mice. Intraperitoneal injection of anti-CD3 antibody into Malt1 PD mouse induced less productions of IL-17 in the plasma, as well as the colonic gene expression of IL-17A, compared with WT mice, whereas IFN-gamma production was not impaired. In naive T-cell transfer colitis model, Malt1 PD T cells induced less disease severity than WT T cells. Then, reduction in the populations of Th17 and Th1/17 cells was observed in the mesenteric lymph nodes of the recipient mice transferred with Malt1 PD T cells, whereas those of Th1 cells were not impaired. IL-17A expression in the colon was also decreased in the mouse receiving Malt1 PD T cells. CONCLUSIONS: Inactivation of Malt1 protease activity abrogates Th17 and Th1/17 cell activation, resulting in the amelioration of experimental colitis. |
