Natural killer cells in inflammatory heart disease

Ong, SuFey; Rose, Noel R.; Čiháková, Daniela

doi:10.1016/j.clim.2016.11.010

Cited by 85 publications

(77 citation statements)

References 157 publications

(164 reference statements)

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“…NK cells account for over 1% of cardiac lymphocytes and participate to the regulation of process involved in cardiac diseases [ 181 ]. In patients with coronary artery diseases (CAD), NK cells have been found to be decreased in number and function, but not altered in their phenotype [ 182 ].…”

Section: Innate Immunity Cells Contribution To Cardiac Fibrosismentioning

confidence: 99%

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Baci

Bosi

Parisi

et al. 2020

IJMS

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Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in “sterile” inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis.

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Section: Innate Immunity Cells Contribution To Cardiac Fibrosismentioning

confidence: 99%

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Baci

Bosi

Parisi

et al. 2020

IJMS

View full text Add to dashboard Cite

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“…Rose et al suggested that the immunopathogenesis of this myocarditis model has three different stages: (i) induction of pathogenic autoimmunity from virus infection; (ii) development of myocardial inflammation; and (iii) progression to dilated cardiomyopathy. Each of the three stages has a cytokine signature and inflammatory cell profile that mirrors and modulates the quantity and quality of inflammation and healing …”

Section: Animal Modelsmentioning

confidence: 99%

Inflammation in myocardial disease: From myocarditis to dilated cardiomyopathy

Imanaka‐Yoshida

2019

Pathology International

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Dilated cardiomyopathy (DCM) is a heterogeneous group of myocardial diseases clinically defined by the presence of left ventricular dilatation and contractile dysfunction. Among various causes of DCM, a progression from viral myocarditis to DCM has long been hypothesized. Supporting this possibility, studies by endomyocardial biopsy, the only method to obtain a definite diagnosis of myocarditis at present, have provided evidence of inflammation in the myocardium in DCM patients. A number of experimental studies have elucidated a cell‐mediated autoimmune mechanism triggered by viral infection in the progression of myocarditis to DCM. In addition, the important role of inflammation in the pathogenesis of heart failure has been recognized, and many terms including myocarditis, inflammatory cardiomyopathy, and inflammatory DCM have been used for myocardial diseases associated with inflammation. This review discusses the pathophysiology of inflammation in the myocardium, and refers to diagnosis and treatment based on these concepts.

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“…However, their activation could also cause autoaggression and inflammation if the host's autologous cells become stressed/infected and become more susceptible to NK cell-mediated killing. Blocking of one or more NK cell activating receptors may alleviate disease progression as has been demonstrated in cardiac inflammation [76]. However, further studies are required to test the relevance of such an approach in CD patients.…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

Phenotypic and Functional Changes in Peripheral Blood Natural Killer Cells in Crohn Disease Patients

Samarani

Sagala

Jantchou

et al. 2020

Mediators of Inflammation

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We investigated activation status, cytotoxic potential, and gut homing ability of the peripheral blood Natural Killer (NK) cells in Crohn disease (CD) patients. For this purpose, we compared the expression of different activating and inhibitory receptors (KIR and non-KIR) and integrins on NK cells as well as their recent degranulation history between the patients and age-matched healthy controls. The study was conducted using freshly obtained peripheral blood samples from the study participants. Multiple color flow cytometry was used for these determinations. Our results show that NK cells from treatment-naïve CD patients expressed higher levels of activating KIR as well as other non-KIR activating receptors vis-à-vis healthy controls. They also showed increased frequencies of the cells expressing these receptors. The expression of several KIR and non-KIR inhibitory receptors tended to decrease compared with the cells from healthy donors. NK cells from the patients also expressed increased levels of different gut-homing integrin molecules and showed a history of increased recent degranulation events both constitutively and in response to their in vitro stimulation. Furthermore, treatment of the patients tended to reverse these NK cell changes. Our results demonstrate unequivocally, for the first time, that peripheral blood NK cells in treatment-naïve CD patients are more activated and are more poised to migrate to the gut compared to their counterpart cells from healthy individuals. Moreover, they show that treatment of the patients tends to normalize their NK cells. The results suggest that NK cells are very likely to play a role in the immunopathogenesis of Crohn disease.

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Natural killer cells in inflammatory heart disease

Cited by 85 publications

References 157 publications

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis

Inflammation in myocardial disease: From myocarditis to dilated cardiomyopathy

Phenotypic and Functional Changes in Peripheral Blood Natural Killer Cells in Crohn Disease Patients

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