{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T01:57:13Z","timestamp":1792547833487,"version":"4.5.0"},"reference-count":121,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2020,12,11]],"date-time":"2020-12-11T00:00:00Z","timestamp":1607644800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Regulatory T cells (Tregs) express the lineage-defining transcription factor FoxP3 and play crucial roles in self-tolerance and immune homeostasis. Thymic tTregs are selected based on affinity for self-antigens and are stable under most conditions. Peripheral pTregs differentiate from conventional CD4 T cells under the influence of TGF-\u03b2 and other cytokines and are less stable. Treg plasticity refers to their ability to inducibly express molecules characteristic of helper CD4 T cell lineages like T-helper (Th)1, Th2, Th17 or follicular helper T cells. Plastic Tregs retain FoxP3 and are thought to be specialized regulators for \u201ctheir\u201d lineage. Unstable Tregs lose FoxP3 and switch to become exTregs, which acquire pro-inflammatory T-helper cell programs. Atherosclerosis with systemic hyperlipidemia, hypercholesterolemia, inflammatory cytokines, and local hypoxia provides an environment that is likely conducive to Tregs switching to exTregs.<\/jats:p>","DOI":"10.3390\/cells9122665","type":"journal-article","created":{"date-parts":[[2020,12,14]],"date-time":"2020-12-14T00:45:36Z","timestamp":1607906736000},"page":"2665","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["Regulatory T Cell Stability and Plasticity in Atherosclerosis"],"prefix":"10.3390","volume":"9","author":[{"given":"Amal J.","family":"Ali","sequence":"first","affiliation":[{"name":"Laboratory of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, San Diego, CA 92037, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey","family":"Makings","sequence":"additional","affiliation":[{"name":"Laboratory of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, San Diego, CA 92037, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9339-3672","authenticated-orcid":false,"given":"Klaus","family":"Ley","sequence":"additional","affiliation":[{"name":"Laboratory of Inflammation Biology, La Jolla Institute for Immunology, 9420, Athena Circle Drive, La Jolla, San Diego, CA 92037, USA"},{"name":"Department of Bioengineering, University of California, 9500 Gilman Drive, MC0412, La Jolla, San Diego, CA 92093, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2020,12,11]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"368","DOI":"10.1038\/nrneph.2017.51","article-title":"The immunology of atherosclerosis","volume":"13","author":"Gistera","year":"2017","journal-title":"Nat. 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