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Innate immune signaling links diverse intracellular pathways in eukaryotic cells, from inflammation to metabolism as well as host defense. In immune cells, mitochondria act as docking sites for innate immune signaling pathways, including those downstream of toll-like receptors (TLRs), whose activation by inflammatory signals contribute to mitochondrial damage. The importance of innate immune signaling in β-cells, however, has been vexing. Deletion of TLRs enhances β-cell mass following diet-induced obesity (DIO), while loss of downstream TLR signaling adaptors impairs β-cell function. Moreover, the regulatory relationships between innate immune signaling and mitochondrial quality control responses to mitochondrial damage are unclear. Here, we observe that the E3 ubiquitin ligase Traf6, which is central to the transmission of TLR-dependent innate immune signals to induce inflammation, surprisingly …