Expression of Markers of Regulatory CD4+CD25+foxp3+ Cells in Atherosclerotic Plaques of Human Coronary Arteries

Abstract

The content of marker foxp3 of regulatory T cells and chemokines in atherosclerotic plaques of human coronary arteries was measured by the polymerase chain reaction. In vitro migration of regulatory CD4(+)CD25(+)foxp3(+) cells in the CD4(+) lymphocyte population from healthy donors was studied after treatment with chemokines I-309, IP-10, and SDF-1. mRNA for the factor foxp3 and chemokines SDF-1, I-309, and MIP-1beta were found in the majority of samples from atherosclerotic plaques. SDF-1 induced maximum migratory response of CD4(+)CD25(+)foxp3(+) cells.

Effect of serum amyloid A1 treatment on global gene expression in THP-1-derived macrophages

“…Genes that are upregulated by SAA1 treatment such as cytokines, chemokines, CD40 [30], CD44, and OLR1 are potentially atherogenic. CCL1 and CCL4 are both stimulators of macrophage migration into tissues [31,32] and are found in the majority of samples from atherosclerotic plaques of human coronary arteries [33]. Increased production of OLR1 can facilitate the formation of foam cells [34].…”

CC and CXC chemokines are pivotal mediators of cerebral injury in ischaemic stroke

“…This concept was supported the beneficial role of CXCL12 in tissue reparation via the recruitment of mesenchymal stem cells (85). CXCL12 mRNA expression was detected in human atherosclerotic plaques as well as in developing and mature CNS (86)(87)(88). Importantly, CXCR7 expression was increased in the brain (mainly in ischaemic regions) after an ischaemic stroke, thus amplifying CXCL12-mediated functions (89).…”

The Prognostic Impact of Circulating Regulatory T Lymphocytes on Mortality in Patients with Ischemic Heart Failure with Reduced Ejection Fraction

“…This specific regulatory T cell population plays a pivotal role in fostering immune homeostasis and disruption of function or development is a primary cause of inflammatory and autoimmune diseases, e.g., rheumatoid arthritis. Tregs have been documented in inflammatory or damaged muscle tissue and atherosclerotic plaques [35,36]. Through the secretion of anti-inflammatory cytokines such as TGF-b, IL-10, and IL-35, they prevent further progression of atherosclerosis and postinfarction inflammation [37][38][39].…”