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Crosstalk Between Dendritic Cells and T Lymphocytes During Atherogenesis: Focus on Antigen Presentation and Break of Tolerance

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Abstract

Atherosclerosis is a chronic disease resulting from an impaired lipid and immune homeostasis, where the interaction between innate and adaptive immune cells leads to the promotion of atherosclerosis-associated immune-inflammatory response. Emerging evidence has suggested that this response presents similarities to the reactivity of effector immune cells toward self-epitopes, often as a consequence of a . In this context, dendritic cells, a heterogeneous population of antigen presenting cells, play a key role in instructing effector T cells to react against foreign antigens and T regulatory cells to maintain tolerance against self-antigens and/or to patrol for self-reactive effector T cells. Alterations in this delicate balance appears to contribute to atherogenesis. The aim of this review is to discuss different DC subsets, and their role in atherosclerosis as well as in T cell polarization. Moreover, we will discuss how loss of T cell tolerogenic phenotype participates to the immune-inflammatory response associated to atherosclerosis and how a better understanding of these mechanisms might result in designing immunomodulatory therapies targeting DC-T cell crosstalk for the treatment of atherosclerosis-related inflammation.

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References
1.
Wolf D, Gerhardt T, Winkels H, Michel N, Pramod A, Ghosheh Y . Pathogenic Autoimmunity in Atherosclerosis Evolves From Initially Protective Apolipoprotein B-Reactive CD4 T-Regulatory Cells. Circulation. 2020; 142(13):1279-1293. PMC: 7515473. DOI: 10.1161/CIRCULATIONAHA.119.042863. View

2.
Flynn M, Pernes G, Lee M, Nagareddy P, Murphy A . Monocytes, Macrophages, and Metabolic Disease in Atherosclerosis. Front Pharmacol. 2019; 10:666. PMC: 6584106. DOI: 10.3389/fphar.2019.00666. View

3.
Wick G, Jakic B, Buszko M, Wick M, Grundtman C . The role of heat shock proteins in atherosclerosis. Nat Rev Cardiol. 2014; 11(9):516-29. DOI: 10.1038/nrcardio.2014.91. View

4.
Nilsson J, Shah P . Promoting athero-protective immunity by vaccination with low density lipoprotein-derived antigens. Atherosclerosis. 2021; 335:89-97. DOI: 10.1016/j.atherosclerosis.2021.08.033. View

5.
Watanabe M, Sangawa A, Sasaki Y, Yamashita M, Tanaka-Shintani M, Shintaku M . Distribution of inflammatory cells in adventitia changed with advancing atherosclerosis of human coronary artery. J Atheroscler Thromb. 2008; 14(6):325-31. DOI: 10.5551/jat.e489. View