Dendritic cells (DCs) must integrate a broad array of environmental cues to exact control over downstream immune responses including T polarization. The multienzyme aminoacyl-tRNA synthetase complex component AIMp1/p43 responds to cellular stress and exerts pro-inflammatory functions; however, a role for DC-expressed AIMp1 in T polarization has not previously been shown. Here, we demonstrate that the absence of AIMp1 in bone marrow-derived DC (BMDC) significantly impairs cytokine and costimulatory molecule expression, p38 MAPK signaling, and T1 polarization of cocultured T-cells while significantly dysregulating immune-related gene expression.
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