Journal
JOURNAL OF IMMUNOLOGY
Volume 205, Issue 4, Pages 981-986Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000057
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Funding
- National Natural Science Foundation of China [31500699]
- China Postdoctoral Science Foundation [2016M602146]
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Optimal activation of TLR pathways is crucial for the initiation of inflammatory responses and eliminating invading microorganisms. 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-KB 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.
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