Abstract
Abstract Dendritic Cells (DCs) are considered the most potent antigen-presenting cells due to their superior capacity to cross-present exogenous antigens to CD8 T cells for effective adaptive immunity. They internalize foreign antigens by phagocytosis, receptor-mediated endocytosis or macropinocytosis, which are then processed in endo/lysosomal compartments and loaded on MHC class I. However, the molecular mechanisms regulating exogenous antigen uptake and cross-presentation by DCs remain unclear. We revealed a potential regulatory role of an RNA-binding protein, Quaking (QKI), in antigen presentation. Our previous studies in neural stem cells and microglia identified QKI as a novel regulator of phagosome maturation and endosome signaling via interaction with the transcription factor PPARβ/δ. Therefore, we hypothesize that QKI, together with PPARβ/δ enhances DC antigen uptake and cross-presentation via promoting phagosome and endolysosome signaling. We found QKI and PPARβ/δ to be significantly unregulated in human monocyte-derived DCs, and demonstrated that activating the QKI-PPARβ/δ complex in DCs upregulates QKI targets and significantly promotes DC phagocytosis activity, suggesting QKI cooperates with PPARβ/δ to enhance antigen uptake. The biological role of QKI in antigen cross-presentation and the effect of QKI enhancement on induction of CD8 T cell response by DC are currently under investigation. Understanding the role of QKI in DC may reveal how antigen presentation is regulated and provide new strategies to improve DC-based immunotherapy.
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