Restricting TRIM13 sustains dendritic cell immunity through STING signaling during sepsis. (IMAGE)
Caption
Restricting TRIM13 sustains dendritic cell immunity through STING signaling during sepsis. Schematic overview of how TRIM13 regulates dendritic cell (DC) function and immune outcomes during sepsis. In wild-type mice, sepsis induces TRIM13-dependent ER-associated degradation (ERAD) and ER-phagy, promoting STING degradation and limiting downstream IRF3 activation, inflammasome priming, and antigen presentation. This process drives DCs toward an immunosuppressive state, resulting in reduced T-cell activation, impaired organ recovery, and lower survival. In contrast, DC-specific Trim13 deficiency disrupts ERAD- and ER-phagy–mediated STING turnover, leading to sustained STING signaling, transient early DC pyroptosis, and enhanced antigen presentation. Over time, this preserves proinflammatory cytokine production, promotes T-cell activation, improves organ function, and ultimately increases overall survival following sepsis.
Credit
Burns & Trauma
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CC BY