TLR-dependent phagosome tubulation in dendritic cells promotes phagosome cross-talk to optimize MHC-II antigen presentation

摘要: Dendritic cells (DCs) phagocytose large particles like bacteria at sites of infection and progressively degrade them within maturing phagosomes. Phagosomes in DCs are also signaling platforms for pattern recognition receptors, such as Toll-like receptors (TLRs), assembly cargo-derived peptides with major histocompatibility complex class II (MHC-II) molecules. Although TLR from phagosomes stimulates presentation phagocytosed antigens, the mechanisms underlying this enhancement cell surface delivery MHC-II–peptide complexes not known. We show that DCs, extend numerous long tubules several hours after phagocytosis. Tubule formation requires an intact microtubule actin cytoskeleton MyD88-dependent phagosomal signaling, but phagolysosome or extensive proteolysis. In contrast to emerge endolysosomes uptake soluble ligands stimulation, late-onset essential phagosome-derived plasma membrane. Rather, tubulation promotes MHC-II by enabling maximal cargo transfer among bear a signature. Our data functionally distinct those lysosomes unique adaptations phagocytic machinery facilitate exchange antigen TLR-signaling