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Macrophages and immune cells in atherosclerosis: recent advances and novel concepts

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Abstract

Atherosclerotic lesion-related thrombosis is the major cause of myocardial infarction and stroke, which together constitute the leading cause of mortality worldwide. The inflammatory response is considered as a predominant driving force in atherosclerotic plaque formation, growth and progression towards instability and rupture. Notably, accumulation of macrophages in the intima and emergence of a pro-inflammatory milieu are a characteristic feature of plaque progression, and these processes can be modulated by adaptive immune responses. Recently, novel evidences of onsite proliferation of macrophages in lesions and transdifferentiation of smooth muscle cells to macrophages have challenged the prevalent paradigm that macrophage accumulation mostly relies on recruitment of circulating monocytes to plaques. Furthermore, previously unrecognized roles of inflammatory cell subsets such as plasmacytoid dendritic cells, innate response activator B cells or CD8+ T cells in atherosclerosis have emerged, as well as novel mechanisms by which regulatory T cells or natural killer T cells contribute to lesion formation. Here, we review and discuss these recent advances in our understanding of inflammatory processes in atherosclerosis.

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Acknowledgments

This work was supported by the Deutsche Forschungsgemeinschaft (SFB688 TPA22, and ZE 827/1-2 to A.Z.).

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On behalf of all authors, the corresponding author states that there is no conflict of interest.

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Cochain, C., Zernecke, A. Macrophages and immune cells in atherosclerosis: recent advances and novel concepts. Basic Res Cardiol 110, 34 (2015). https://doi.org/10.1007/s00395-015-0491-8

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