Research ArticleAtherosclerosis

Transforming Growth Factor–β Signaling in T Cells Promotes Stabilization of Atherosclerotic Plaques Through an Interleukin-17–Dependent Pathway

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Science Translational Medicine  31 Jul 2013:
Vol. 5, Issue 196, pp. 196ra100
DOI: 10.1126/scitranslmed.3006133

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IL-17 Helps Plaques Lie Dormant

Like a dormant volcano, stable atherosclerotic plaques can lull you into a false sense of security. The accumulation of lipids and inflammatory mediators results in arterial hardening and lack of flexibility, but individuals with these plaques may be asymptomatic for decades. However, when an unstable plaque ruptures, thrombi forming on the exposed tissue can block blood flow, resulting in heart attack or stroke. Gisterå et al. now report that transforming growth factor–β (TGF-β) promotes plaque stabilization through the effects of interleukin-17 (IL-17).

The authors looked at T cells with enhanced expression of TGF-β in a mouse model of atherosclerosis. They found that these animals had larger atherosclerotic lesions, but these lesions were more stable. Inhibiting IL-17 through neutralizing antibodies decreased the stability of these plaques, whereas IL-17 expression correlated to expression of components of the fibrous cap in human atherosclerotic plaques. These data suggest that patients treated with IL-17 receptor blockers should be closely monitored for cardiovascular events and provide IL-17 as a therapeutic option to prevent plaque eruption.