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Mouse dendritic cells (DCs) can rapidly extend their Class II MHC-positive late endosomal compartments into tubular structures, induced by Toll-like receptor (TLR) triggering. Within antigen-presenting DCs, tubular endosomes polarize toward antigen-specific CD4(+) T cells, which are considered beneficial for their activation. Here we describe that also in human DCs, TLR triggering induces tubular late endosomes, labeled by fluorescent LDL. TLR triggering was insufficient for induced tubulation of transferrin-positive endosomal recycling compartments (ERCs) in human monocyte-derived DCs. We studied endosomal remodeling in human DCs in co-cultures of DCs with CD8(+) T cells. Tubulation of ERCs within human DCs requires antigen-specific CD8(+) T cell interaction. Tubular remodeling of endosomes occurs within 30 min of T cell contact and involves ligation of HLA-A2 and ICAM-1 by T cell-expressed T cell receptor and LFA-1, respectively. Disintegration of microtubules or inhibition of endosomal recycling abolished tubular ERCs, which coincided with reduced antigen-dependent CD8(+) T cell activation. Based on these data, we propose that remodeling of transferrin-positive ERCs in human DCs involves both innate and T cell-derived signals.

Type

Journal article

Journal

The Journal of biological chemistry

Publication Date

01/2014

Volume

289

Pages

520 - 528

Addresses

From the Department of Pediatrics, Laboratory of Translational Immunology, University Medical Center Utrecht, Wilhelmina Children's Hospital, 3584 EA Utrecht, The Netherlands and.

Keywords

Dendritic Cells, CD8-Positive T-Lymphocytes, Monocytes, Cells, Cultured, Endosomes, Animals, Humans, Mice, Intercellular Adhesion Molecule-1, Lymphocyte Function-Associated Antigen-1, HLA-A2 Antigen, Coculture Techniques, Signal Transduction, Immunity, Cellular, Antigen Presentation, Female, Male, Toll-Like Receptors, Immunity, Innate