NDLI: Cell-specific TLR9 trafficking in primary APCs of transgenic TLR9-GFP mice.

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Cell-specific TLR9 trafficking in primary APCs of transgenic TLR9-GFP mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Avalos, Ana M. Brinkmann, Melanie M. Pils, Marina C. Kim, You-Me Oelkers, J. Margit Ottinger, Matthias Jaenisch, Rudolf Ploegh, Hidde L. Kirak, Oktay
Description	Country affiliation: United States Author Affiliation: Avalos AM ( Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.)
Abstract	Recognition of nucleic acids by TLR9 requires its trafficking from the endoplasmic reticulum to endolysosomal compartments and its subsequent proteolytic processing. Both processes depend on interactions of TLR9 with the polytopic endoplasmic reticulum-resident protein UNC93B1. To examine the intracellular behavior of TLR9 in primary APCs, we generated transgenic mice expressing a TLR9-GFP fusion. The TLR9-GFP transgene is functional and is proteolytically processed in resting bone marrow-derived macrophages (BMDMs), dendritic cells, and B cells. Inhibition of cleavage impairs TLR9-dependent responses in all primary APCs analyzed. The kinetics of TLR9-GFP processing in BMDMs and B cells differs: in B cells, proteolysis occurs at a faster rate, consistent with an almost exclusive localization to endolysosomes at the resting state. In contrast to the joint requirement for cathepsins L and S for TLR9 cleavage in macrophages, TLR9-GFP cleavage depends on cathepsin L activity in B cells. As expected, in BMDMs and B cells from UNC93B1 (3d) mutant mice, cleavage of TLR9-GFP is essentially blocked, and the expression level of UNC93B1 appears tightly correlated with TLR9-GFP cleavage. We conclude that proteolysis is a universal requirement for TLR9 activation in the primary cell types tested, however the cathepsin requirement, rate of cleavage, and intracellular behavior of TLR9 varies. The observed differences in trafficking indicate the possibility of distinct modes of endosomal content sampling to facilitate initiation of TLR-driven responses in APCs.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202342
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigen-presenting Cells Metabolism Toll-like Receptor 9 Genetics Animals B-lymphocytes Bone Marrow Cells Cell Line Endoplasmic Reticulum Green Fluorescent Proteins Lysosomes Macrophages Membrane Transport Proteins Mice Mice, Transgenic Protein Stability Protein Transport Proteolysis Signal Transduction Transgenes Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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