The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease

Sarah A Smith, Andriy O Samokhin, Mabruka Alfadi, Emer C Murphy, David Rhodes, W Mike L Holcombe, Endre Kiss-Toth, Robert F Storey, Siu-Pok Yee, Sheila E Francis, Eva E Qwarnstrom

Research output: Contribution to journalArticle (Academic Journal)

Abstract

Expression of the interleukin-1 receptor type I (IL-1RI) co-receptor Toll-like and interleukin-1 receptor regulator (TILRR) is significantly increased in blood monocytes following myocardial infarction and in the atherosclerotic plaque, whereas levels in healthy tissue are low. TILRR association with IL-1RI at these sites causes aberrant activation of inflammatory genes, which underlie progression of cardiovascular disease. The authors show that genetic deletion of TILRR or antibody blocking of TILRR function reduces development of atherosclerotic plaques. Lesions exhibit decreased levels of monocytes, with increases in collagen and smooth muscle cells, characteristic features of stable plaques. The results suggest that TILRR may constitute a rational target for site- and signal-specific inhibition of vascular disease.

Original languageEnglish
Pages (from-to)398-414
Number of pages17
JournalJACC: Basic to Translational Science
Volume2
Issue number4
DOIs
Publication statusPublished - Aug 2017

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