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Foxp3+ Regulatory T Cells Play a Protective Role in Angiotensin II-Induced Aortic Aneurysm Formation in Mice.
- Source :
- Hypertension (0194911X); Apr2015, Vol. 65 Issue 4, p889-895, 7p
- Publication Year :
- 2015
-
Abstract
- Although regulatory T cells (Tregs) have been shown to play a protective role in abdominal aortic aneurysm (AAA) formation, it remains unclear whether expansion of endogenous Foxp3<superscript>+</superscript> Tregs prevents AAA. In the current study, we determined the effects of endogenous Foxp3<superscript>+</superscript> Treg expansion or depletion in an experimental model of AAA. We continuously infused 12-week-old apolipoprotein E-deficient mice fed a high-cholesterol diet with angiotensin II (n=60) or normal saline (n=12) by implanting osmotic mini-pumps and evaluated AAA formation at 16 weeks. The angiotensin II-infused mice received interleukin-2/anti-interleukin-2 monoclonal antibody complex (interleukin-2 complex; n=31) or PBS (n=29). Eighty-one percent of angiotensin II-infused mice developed AAA, with 42% mortality possibly because of aneurysm rupture. Interleukin-2 complex treatment systemically increased the number of Foxp3<superscript>+</superscript> Tregs and significantly decreased the incidence (52%) and mortality (17%) of AAA. Immunohistochemical analysis showed reduced accumulation of macrophages and increased numbers of Foxp3<superscript>+</superscript> Tregs in aneurysmal tissues, suggesting that expansion of Tregs may suppress local inflammation in the vessel wall and provide protection against AAA formation. Furthermore, genetic depletion of Foxp3<superscript>+</superscript> Tregs led to a significant increase in the mortality of AAA, suggesting the protective role of Foxp3<superscript>+</superscript> Tregs against AAA. Our findings suggest that Foxp3<superscript>+</superscript> Tregs may play a protective role in AAA formation and that promotion of an endogenous regulatory immune response may be a potentially valuable therapeutic approach for preventing AAA. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 0194911X
- Volume :
- 65
- Issue :
- 4
- Database :
- Supplemental Index
- Journal :
- Hypertension (0194911X)
- Publication Type :
- Academic Journal
- Accession number :
- 102599067
- Full Text :
- https://doi.org/10.1161/HYPERTENSIONAHA.114.04934