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CorrigendumCardiology Free access | 10.1172/JCI19855C1

Th2-predominant inflammation and blockade of IFN-γ signaling induce aneurysms in allografted aortas

Koichi Shimizu, Masayoshi Shichiri, Peter Libby, Richard T. Lee, and Richard N. Mitchell

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First published September 1, 2004 - More info

Published in Volume 114, Issue 5 on September 1, 2004
J Clin Invest. 2004;114(5):739–739. https://doi.org/10.1172/JCI19855C1.
© 2004 The American Society for Clinical Investigation
First published September 1, 2004 - Version history

Related article:

Th2-predominant inflammation and blockade of IFN-γ signaling induce aneurysms in allografted aortas
Koichi Shimizu, … , Richard T. Lee, Richard N. Mitchell
Koichi Shimizu, … , Richard T. Lee, Richard N. Mitchell
Categories: Article Cardiology

Th2-predominant inflammation and blockade of IFN-γ signaling induce aneurysms in allografted aortas

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Abstract

Abdominal aortic aneurysms (AAAs) cause death due to complications related to expansion and rupture. The underlying mechanisms that drive AAA development remain largely unknown. We recently described evidence for a shift toward T helper type 2 (Th2) cell responses in human AAAs compared with stenotic atheromas. To evaluate putative pathways in AAA formation, we induced Th1- or Th2-predominant cytokine environments in an inflammatory aortic lesion using murine aortic transplantation into WT hosts or those lacking the receptors for the hallmark Th1 cytokine IFN-γ, respectively. Allografts in WT recipients developed intimal hyperplasia, whereas allografts in IFN-γ receptor–deficient (GRKO) hosts developed severe AAA formation associated with markedly increased levels of MMP-9 and MMP-12. Allografts in GRKO recipients treated with anti–IL-4 antibody to block the characteristic IL-4 Th2 cytokine or allografts in GRKO hosts also congenitally deficient in IL-4 did not develop AAA and likewise exhibited attenuated collagenolytic and elastolytic activities. These observations demonstrate an important dichotomy between cellular immune responses that induce IFN-γ– or IL-4–dominated cytokine environments. The findings establish important regulatory roles for a Th1/Th2 cytokine balance in modulating matrix remodeling and have important implications for the pathophysiology of AAAs and arteriosclerosis.

Authors

Koichi Shimizu, Masayoshi Shichiri, Peter Libby, Richard T. Lee, Richard N. Mitchell

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Original citation: J. Clin. Invest.114:300–308(2004). doi:10.1172/JCI19855.

Citation for this Corrigendum: J. Clin. Invest.114:739 (2004). doi:10.1172/JCI19855C1.

One of the NIH grants that appear in the Acknowledgments section was cited incorrectly as “HL-67283 (to K. Shimizu and R.N. Mitchell)”. The correct NIH grant citation is “HL-67249 (to K. Shimizu and R.N. Mitchell)”

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