Despite the skepticism that once prevailed among immunologists, it is now widely accepted that the normal immune system harbors a T-cell population, called regulatory T cells (Treg cells), specialized for immune suppression. It was first shown that depletion of a T-cell subpopulation from normal rodents produced autoimmune disease. Search for a molecular marker specific for such autoimmune-preventive Treg cells has revealed that the majority, if not all, of them constitutively express the CD25 molecule as depletion of CD25+CD4+ T cells spontaneously evokes autoimmune disease in otherwise normal rodents. The expression of CD25 by Treg cells has made it possible to delineate their developmental pathways, in particular their thymic development, and establish simple in vitro assay for assessing their suppressive activity. The marker and the in vitro assay have helped to identify human Treg cells with similar functional and phenotypic characteristics. Recent efforts have shown that natural Treg cells specifically express the transcription factor Foxp3 and that mutations of the Foxp3 gene produce a variety of immunological diseases in humans and rodents. Specific expression of Foxp3 in natural Treg cells has enabled their functional and developmental characterization by genetic approach. These studies altogether have provided firm evidence for Foxp3+CD25+CD4+ Treg cells as an indispensable cellular constituent of the normal immune system for establishing and maintaining immunologic self-tolerance and immune homeostasis. Treg cells are now within the scope of clinical use to treat immunological diseases and control physiological and pathological immune responses.

Regulatory T Cells

Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets.

MicroRNAs (miRNAs) are a novel class of small, non-coding, single-stranded RNAs that negatively regulate gene expression via translational inhibition or mRNA degradation followed by protein synthesis repression Many miRNAs are expressed in a tissue- and/or cell-specific manner and their expression patterns are reflective of underlying patho-physiologic processes miRNAs can be detected in serum or in plasma in a remarkably stable form, making them attractive biomarkers for human diseases This review describes the progress of identifying circulating miRNAs as novel biomarkers for diverse cardiovascular diseases, including acute myocardial infarction, heart failure, coronary artery disease, diabetes, stroke, essential hypertension, and acute pulmonary embolism In addition, the origin and function and the different strategies to identify circulating miRNAs as novel biomarkers for cardiovascular diseases are also discussed Rarely has an opportunity arisen to advance such new biology for the diagnosis of cardiac diseases

Circulating microRNAs: novel biomarkers for cardiovascular diseases

Platelet-derived chemokines in inflammation and atherosclerosis

Chronic inflammation in response to lipoprotein accumulation in the arterial wall is central in the development of atherosclerosis. Both innate and adaptive immunity are involved in this process. Adaptive immune responses develop against an array of potential antigens presented to effector T lymphocytes by antigen-presenting cells, especially dendritic cells. Functional analysis of the role of different T-cell subsets identified the Th1 responses as proatherogenic, whereas regulatory T-cell responses exert antiatherogenic activities. The effect of Th2 and Th17 responses is still debated. Atherosclerosis is also associated with B-cell activation. Recent evidence established that conventional B-2 cells promote atherosclerosis. In contrast, innate B-1 B cells offer protection through secretion of natural IgM antibodies. This review discusses the recent development in our understanding of the role of T- and B-cell subsets in atherosclerosis and addresses the role of dendritic cell subpopulations in the control of adaptive immunity.

Adaptive (T and B cells) immunity and control by dendritic cells in atherosclerosis

The upregulation of Th1 cells has been suggested to have an essential function in the development of atherosclerosis (AS) Recent studies indicate that miR-146a is a microRNA specifically and highly expressed in Th1-driven autoimmune disease The aim of the study was to investigate the possible mechanisms of the miR-146a in the onset of acute coronary syndrome (ACS) The results showed that the expression of miR-146a in peripheral blood mononuclear cells (PBMCs) was significantly increased in patients with ACS We showed that overexpression of miR-146a in PBMCs could significantly upregulate the function of Th1 cells Furthermore, we showed that miR-146a treatment could modulate the Th1 differentiation through posttranscriptional enhancing the T-bet pathway in PBMCs In addition, this study also provided evidence that miR-146a treatment in vitro could induce the protein expression of TNF-alpha, MCP-1, NF-kappaB p65, which are key pro-inflammatory cytokines and critical transcription factor in AS In contrast, miR-146a inhibitor could attenuate these phenomena significantly The results support the concept that miR-146a may be a novel regulatory factor in Th1 differentiation and a new therapeutic target for AS and ACS

miR-146a in PBMCs modulates Th1 function in patients with acute coronary syndrome.

Overexpression of CXCL16 promotes a vulnerable plaque phenotype in Apolipoprotein E–Knockout Mice

Background
The crucial role of T helper (Th) cells and chronic inflammation in atherosclerosis and coronary artery disease is no longer controversial. Evidence has revealed that Th cell type 1 (Th1) is closely associated with the pathogenesis of acute coronary syndrome (ACS). But the mechanisms involved in the generation of Th1 cells have not been fully elucidated. IFN regulatory factor (IRF)-1 is a pleiotropic transcription factor involved in innate immunity and chronic inflammation disease. The study was undertaken to investigate the potential effect of IRF-1 on the Th1 cell function in patients with ACS in vitro.

Inhibition of IFN Regulatory Factor-1 Down-Regulate Th1 Cell Function in Patients with Acute Coronary Syndrome

Downregulation of T helper cell type 3 in patients with acute coronary syndrome.

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Papers

miR-146a in PBMCs modulates Th1 function in patients with acute coronary syndrome.

Overexpression of CXCL16 promotes a vulnerable plaque phenotype in Apolipoprotein E–Knockout Mice

Inhibition of IFN Regulatory Factor-1 Down-Regulate Th1 Cell Function in Patients with Acute Coronary Syndrome

Downregulation of T helper cell type 3 in patients with acute coronary syndrome.