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

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 wit...

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Main Authors:	Sarah A. Smith, PhD, Andriy O. Samokhin, PhD, Mabruka Alfadi, PhD, Emer C. Murphy, PhD, David Rhodes, MSc, W. Mike L. Holcombe, PhD, Endre Kiss-Toth, PhD, Robert F. Storey, BSc, BM, DM, Siu-Pok Yee, PhD, Sheila E. Francis, PhD, Eva E. Qwarnstrom, PhD
Format:	Article
Language:	English
Published:	Elsevier 2017-08-01
Series:	JACC: Basic to Translational Science
Subjects:	heparan sulfate proteoglycan interleukin-1 receptor IL-1RI NF-κB TILRR
Online Access:	http://www.sciencedirect.com/science/article/pii/S2452302X1730133X

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spelling	doaj-b66cef1d0265487f8eef2f4e9f8cc4bc2020-11-24T22:34:55ZengElsevierJACC: Basic to Translational Science2452-302X2017-08-012439841410.1016/j.jacbts.2017.03.014The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular DiseaseSarah A. Smith, PhD0Andriy O. Samokhin, PhD1Mabruka Alfadi, PhD2Emer C. Murphy, PhD3David Rhodes, MSc4W. Mike L. Holcombe, PhD5Endre Kiss-Toth, PhD6Robert F. Storey, BSc, BM, DM7Siu-Pok Yee, PhD8Sheila E. Francis, PhD9Eva E. Qwarnstrom, PhD10Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Computer Science, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Cell Biology, University of Connecticut, Farmington, ConnecticutDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomDepartment of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, United KingdomExpression 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.http://www.sciencedirect.com/science/article/pii/S2452302X1730133Xheparan sulfate proteoglycaninterleukin-1 receptorIL-1RINF-κBTILRR
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Sarah A. Smith, PhD Andriy O. Samokhin, PhD Mabruka Alfadi, PhD Emer C. Murphy, PhD David Rhodes, MSc W. Mike L. Holcombe, PhD Endre Kiss-Toth, PhD Robert F. Storey, BSc, BM, DM Siu-Pok Yee, PhD Sheila E. Francis, PhD Eva E. Qwarnstrom, PhD
spellingShingle	Sarah A. Smith, PhD Andriy O. Samokhin, PhD Mabruka Alfadi, PhD Emer C. Murphy, PhD David Rhodes, MSc W. Mike L. Holcombe, PhD Endre Kiss-Toth, PhD Robert F. Storey, BSc, BM, DM Siu-Pok Yee, PhD Sheila E. Francis, PhD Eva E. Qwarnstrom, PhD The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease JACC: Basic to Translational Science heparan sulfate proteoglycan interleukin-1 receptor IL-1RI NF-κB TILRR
author_facet	Sarah A. Smith, PhD Andriy O. Samokhin, PhD Mabruka Alfadi, PhD Emer C. Murphy, PhD David Rhodes, MSc W. Mike L. Holcombe, PhD Endre Kiss-Toth, PhD Robert F. Storey, BSc, BM, DM Siu-Pok Yee, PhD Sheila E. Francis, PhD Eva E. Qwarnstrom, PhD
author_sort	Sarah A. Smith, PhD
title	The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease
title_short	The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease
title_full	The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease
title_fullStr	The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease
title_full_unstemmed	The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease
title_sort	il-1ri co-receptor tilrr (frem1 isoform 2) controls aberrant inflammatory responses and development of vascular disease
publisher	Elsevier
series	JACC: Basic to Translational Science
issn	2452-302X
publishDate	2017-08-01
description	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.
topic	heparan sulfate proteoglycan interleukin-1 receptor IL-1RI NF-κB TILRR
url	http://www.sciencedirect.com/science/article/pii/S2452302X1730133X
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The IL-1RI Co-Receptor TILRR (FREM1 Isoform 2) Controls Aberrant Inflammatory Responses and Development of Vascular Disease

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