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

. 2019 Dec 5;217(1):e20190459. doi: 10.1084/jem.20190459

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

© 2019 Chen 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/).

PMC Copyright notice

Figure 2. — Type-I IFNs affect atherosclerosis. Type-I IFNs can be produced by monocytes, macrophages, pDCs, eosinophils, and B cells and LDGs in autoimmune patients. Locally and systemically elevated type-I IFNs result in increased foam cell formation, EC dysfunction, suppressed EPC maturation, enhanced NETosis, increased monocyte and neutrophil recruitment, and elevated immune cell activation. IFN-stimulated T cells exert stronger cytotoxic function to SMC via TRAIL. Myeloid APCs including macrophages and mDCs secrete higher levels of TNF, leading to IFN-β expression in ECs. Type-I IFN priming of IFN-producing cells such as pDCs, monocytes, B cells, ECs, and LDGs results in an autocrine feedback loop that exacerbates the pro-inflammatory microenvironment.