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. 2019 Nov 28;10:2795. doi: 10.3389/fimmu.2019.02795

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Copyright © 2019 Albany, Trevelin, Giganti, Lombardi and Scottà.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Suppressive mechanisms of Tregs in atherosclerosis. Tregs can directly produce suppressive cytokines and degradative enzymes such as perforin and granzyme that leads to apoptosis. Furthermore, Tregs have been observed to have direct effects on APC's via interaction with via CTLA-4, PD-L1/2, and LAG-3. They can also skew monocyte class switching, encouraging anti-inflammatory M2 macrophages formation which produced collagen and stabilizes the plaque. They can also decrease foam cell formation via the down-regulation of CD36 and CD204.