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. 2018 Apr 2;215(4):1245–1265. doi: 10.1084/jem.20162042

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© 2018 Carpier et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 8. — Schematic representation: LAT is internalized in early/recycling endosomes and traffics back to the immune synapse through a Rab6- and Syntaxin-16–dependent endosomes to Golgi–trans-Golgi retrograde pathway. LAT constitutively recycles from the plasma membrane to early/recycling endosomes. Our data suggest that vesicles from this compartment undergo a retrograde transport to the Golgi apparatus, which is increased upon TCR activation. Rab6 and Syntaxin-16, which play a key role in endosomes to Golgi–trans-Golgi retrograde pathway, are required for the resecretion of LAT containing vesicles to the immune synapse. Indeed, in the absence of these two molecules, LAT is not recruited to the immune synapse. We propose that this retrograde pathway allows the recycling pool of LAT to meet the VAMP7 vesicular SNARE present in the Golgi–trans-Golgi membranes, which is necessary for the polarized transport of LAT to the TCR activation site. This polarized secretion of LAT and perhaps of other molecules controlled by the endosomes to Golgi–trans-Golgi retrograde route plays a key role in T cell activation as shown by the defective TCR stimulation of T lymphocytes lacking Rab6 and Syntaxin-16.