Statins Induce Regulatory T Cell Recruitment via a CCL1 Dependent Pathway

Mira, Emilia; León, Beatriz; Barber, Domingo F.; Jiménez-Baranda, Sonia; Goya, Íñigo; Almonacid, Luis; Márquez, Gabriel; Zaballos, Ángel; Martı́nez-A, Carlos; Stein, Jens V; Ardavı́n, Carlos; Mañes, Santos

doi:10.4049/jimmunol.181.5.3524

Cited by 82 publications

(63 citation statements)

References 53 publications

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“…For instance, Cxcl9 and Cxcl10 (IP-10) are secreted in response to interferon-gamma signalling and are thought to bind to their cognate receptor CCR10 and recruit Th1, Th17 and NKT cells [37]. Ccl1 attracts mainly Treg-like cells [38] and binds to the CCR8 receptor on Th2, Treg and γδT cells [37]. Therefore, immediately upon activation CD4 + T cells secrete a potent cocktail of cytokines and chemokines to recruit other cell types to the site of infection and thus stimulate the adaptive immune response.…”

Section: Discussionmentioning

confidence: 99%

Discovery and characterization of new transcripts from RNA-seq data in mouse CD4+ T cells

et al. 2012

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Despite the routine application of RNA-seq technology to profile cellular transcriptomes and report novel splice variants, the identification and validation of new transcripts remain underexplored. We prepared two RNA-seq libraries from resting and T cell receptor-stimulated mouse CD4(+) T cells. Transcripts unknown to Ensembl represent as much as 5% of the assembled transcripts and are robustly expressed but do not show the same degree of evolutionary conservation or exon distribution of known transcripts, or of novel splice isoforms. Here we present a straightforward and generally applicable computational/experimental workflow that we apply to characterise and experimentally validate 23 mouse transcripts from the RNA-seq libraries that were uncharacterised by Ensembl. Of these, 7 are not supported by any transcript database and therefore are likely to encode new messages. Furthermore, we also report the fast up-regulation of important regulatory molecules only 4 h post-stimulation of the T cell receptor, which calls for a more detailed investigation into early CD4(+) T cell activation mechanisms.

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Section: Discussionmentioning

confidence: 99%

Discovery and characterization of new transcripts from RNA-seq data in mouse CD4+ T cells

et al. 2012

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“…Another examples are statins, inhibitors of 3-hydroxy-3-methylglutaryl CoA reductase, which have been associated with the reduction of cholesterol synthesis, antiatherogenic, and tissue-protective functions, and thus, widely used in the treatment of cardiovascular diseases [93]. Statins have been shown to inhibit T-cell activation and also the recruitment of regulatory T cells [94][95][96]. Statins are also involved in the inhibition of macrophage infiltration and proliferation by modulating the expression of IL-10 and heme oxygenase-1 on these cells [72,97].…”

Section: Mineralocorticoid Receptor-independent Mechanisms In the Modmentioning

confidence: 98%

Aldosterone as a modulator of immunity

Herrada

Campino²,

Amador

et al. 2011

Journal of Hypertension

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High plasmatic levels of aldosterone cause hypertension and contribute to progressive organ damage to the heart, vasculature, and kidneys. Recent studies have demonstrated a role for the immune system in these pathological processes. Aldosterone promotes an inflammatory state characterized by vascular infiltration of immune cells, reactive oxidative stress, and proinflammatory cytokine production. Further, cells of the adaptive immune system, such as T cells, seem to participate in the genesis of mineralocorticoid hormone-induced hypertension. In addition, the observation that aldosterone can promote CD4⁺ T-cell activation and Th17 polarization suggests that this hormone could contribute to the onset of autoimmunity. Here we discuss recent evidence supporting a significant involvement of the immune system, especially adaptive immunity, in the genesis of hypertension and organ damage induced by primary aldosteronism. In addition, possible new therapeutic approaches consisting of immunomodulator drugs to control exacerbated immune responses triggered by elevated aldosterone concentrations will be described.

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“…8 -11 Furthermore, Tregs have the ability to traffic to ar-eas of inflammation to mitigate immune reactions. 12,13 In addition to Tregs' widely known ability to prevent effector T cell proliferation and function, Tregs can suppress the innate immune response. 14 -20 In vivo, CD4 ϩ -CD25 ϩ FoxP3 ϩ Tregs inhibit Adriamycininduced macrophage accumulation and kidney injury and, in vitro, suppress the macrophage inflammatory phenotype.…”

mentioning

confidence: 99%