Interplay of NK cells and monocytes in vascular inflammation and myocardial infarction

Abstract

Inflammatory monocytes and macrophages have been identified as key players in the pathogenesis of atherosclerosis, arterial hypertension, and myocardial infarction (MI). They become powerful mediators of vascular inflammation through their capacity to secrete and induce the production of proinflammatory cytokines, chemokines and adhesion molecules and through the production of reactive oxygen species mainly via their NADPH oxidase. Importantly, a crosstalk exists between NK cells and monocytes that works via a feedforwad amplification loop of T-bet/Interferon-gamma/interleukin-12 signaling, that causes mutual activation of both NK cells and monocytes and that fosters recruitment of inflammatory cells to sites of inflammation. Recently, we have discovered that this crosstalk is crucial for the unrestricted development of angiotensin II (ATII) induced vascular injury in arterial hypertension, the most important risk factor for atherosclerosis and cardiovascular disease worldwide. In this review, we will also discuss possible implications of this interplay between NK cells and monocytes for the pathogenesis of coronary atherosclerosis and myocardial infarction and potential therapeutic options.

Relation between lymphocyte to monocyte ratio and short‐term mortality in patients with acute pulmonary embolism

“…14 Also, Kaya et al showed that soluble CD40 ligand was elevated in acute PE. 23 Cytokines and several proteins such as monocyte chemoattractant protein-1 (MCP-1), CCL2, interferon-inducible protein (IP-10; CXCL10), interleukin-8 cause the migration of monocytes into the vascular wall, subsequent endothelial dysfunction, impact on nitric oxide and endothelin-1 and smooth muscle cell proliferation. Moreover, these data may support the role of inflammation in acute PE.…”

IL-2/Anti–IL-2 Antibody Complex Treatment Inhibits the Development but Not the Progression of Herpetic Stromal Keratitis

“…Although the link between type I interferon and NK cells in controlling corneal HSV-1 infection is not clear, it is reported that in vaccinia viral infection, Type I interferon action on NK cells enhance its effector function and thereby help the NK cells in promoting the viral clearance from infected tissues (33). Similarly, interplay between NK cells and inflammatory monocytes has recently been shown to promote vascular inflammation (34). It is possible that collective interactions between type I interferon, NK cells and inflammatory monocytes help in effectively controlling HSV-1 load in cornea at early time-point post-infection.…”

Natural killer cells in inflammatory heart disease

“…Crosstalk between monocytes and NK cells infiltrating the infarcted tissue can drive a T-bet/IFNγ/IL-12 signaling loop that results in the activation of both cellular populations and the increased recruitment of other inflammatory cells. Furthermore, this crosstalk was required for angiotensin-II induced vascular injury [10, 72]. …”

“…However, blockade of NK cells and their receptors can protect against inflammation and damage in animal models of cardiac injury and inflammation. In these models, NK cells suppress the maturation and trafficking of inflammatory cells, alter the local cytokine and chemokine environments, and induce apoptosis in nearby resident and hematopoietic cells [1, 9, 10]. This review will dissect each protective mechanism employed by NK cells and explore how their properties might be exploited for their therapeutic potential.…”