Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2017 Jun 23;14:21. doi: 10.1186/s12989-017-0202-8

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

PMC Copyright notice

Fig. 6 — Scheme summarizing the single-hit mechanism of IL-1β secretion by steady-state DCs exposed to food-grade SAS particles. In immature DCs, pro-IL-1β is not expressed, but its induction takes place upon uptake of SAS particles into endosomes and MyD88-dependent TLR signaling. Cleavage of the newly expressed pro-IL-1β precursor by the inflammasome-associated caspase leads to IL-1β secretion. In addition, the immature DCs undergo maturation involving shifts in multiple surface markers. IL-1β secretion in response to SAS particles is suppressed by cytochalasin or rottlerin (inhibitors of actin-dependent macropinocytosis), by chloroquine or bafilomycin A (inhibitors of endosomal TLR activation), by genetic ablation of MyD88 (the central adapter of TLR signaling) and by Z-VAD (an inhibitor of the inflammasome-associated caspase)