| First Author | Jiang G | Year | 2020 |
| Journal | J Immunol | Volume | 205 |
| Issue | 4 | Pages | 981-986 |
| PubMed ID | 32611726 | Mgi Jnum | J:300677 |
| Mgi Id | MGI:6502371 | Doi | 10.4049/jimmunol.2000057 |
| Citation | Jiang G, et al. (2020) Tob2 Inhibits TLR-Induced Inflammatory Responses by Association with TRAF6 and MyD88. J Immunol 205(4):981-986 |
| abstractText | Optimal activation of TLR pathways is crucial for the initiation of inflammatory responses and eliminating invading micro-organisms. However, excessive of TLR activation may lead to autoimmune and inflammatory diseases. Thus, TLR pathways should be tightly controlled. In this study, we identify Tob2, a Tob/BTG family member, as a suppressor of TLR pathways. Tob2 deficiency enhances TLR-induced NF-kappaB and MAPK activation and promotes the expression of proinflammatory cytokines in primary peritoneal macrophages of C57BL/6 mice. Furthermore, Tob2-defective C57BL/6 mice may be more susceptible to endotoxemic shock in vivo. Mechanistically, Tob2 interacts with TRAF6 and MyD88 and thus inhibits signaling from the MyD88-TRAF6 complex in primary peritoneal macrophages and HEK293T cells. Therefore, our results uncover a regulatory mechanism of TLR pathways and provide a potential target for the intervention of diseases with excessive TLR activation. |
