Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy

Zhao, Lei; Fu, Zhen-Yan

doi:10.1155/2018/5301548

Cited by 44 publications

(26 citation statements)

References 177 publications

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“…Although there is little doubt that dysregulated, excessive, or prolonged inflammatory responses precipitate or worsen heart failure in human patients, the relative contribution of inflammatory signaling likely depends on the underlying etiology of the disease. In patients developing heart failure due to viral myocarditis, inflammatory injury may be the primary cause of dysfunction and adverse remodeling [5,20]. In contrast, in other heart failure etiologies, the role of inflammatory cytokines is less convincingly documented.…”

Section: Inflammatory Cytokines In the Pathogenesis Of Chronic Heart mentioning

confidence: 99%

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Hanna

Frangogiannis

2020

Cardiovasc Drugs Ther

237

170

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Heart failure exhibits remarkable pathophysiologic heterogeneity. A large body of evidence suggests that regardless of the underlying etiology, heart failure is associated with induction of cytokines and chemokines that may contribute to the pathogenesis of adverse remodeling, and systolic and diastolic dysfunction. The pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 have been extensively implicated in the pathogenesis of heart failure. Inflammatory cytokines modulate phenotype and function of all myocardial cells, suppressing contractile function in cardiomyocytes, inducing inflammatory activation in macrophages, stimulating microvascular inflammation and dysfunction, and promoting a matrixdegrading phenotype in fibroblasts. Moreover, cytokine-induced growth factor synthesis may exert chronic fibrogenic actions contributing to the pathogenesis of heart failure with preserved ejection fraction (HFpEF). In addition to their role in adverse cardiac remodeling, some inflammatory cytokines may also exert protective actions on cardiomyocytes under conditions of stress. Chemokines, such as CCL2, are also upregulated in failing hearts and may stimulate recruitment of pro-inflammatory leukocytes, promoting myocardial injury, fibrotic remodeling, and dysfunction. Although experimental evidence suggests that cytokine and chemokine targeting may hold therapeutic promise in heart failure, clinical translation remains challenging. This review manuscript summarizes our knowledge on the role of TNF-α, IL-1, IL-6, and CCL2 in the pathogenesis of heart failure, and discusses the promises and challenges of targeted anti-cytokine therapy. Dissection of protective and maladaptive cellular actions of cytokines in the failing heart, and identification of patient subsets with overactive or dysregulated myocardial inflammatory responses are required for design of successful therapeutic approaches.

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Section: Inflammatory Cytokines In the Pathogenesis Of Chronic Heart mentioning

confidence: 99%

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Hanna

Frangogiannis

2020

Cardiovasc Drugs Ther

237

170

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“…Так, гистологически миокард пациентов с острым миокардитом характеризуется первичной очаговой клеточной инфильтрацией лимфоцитами, лейкоцитами, моноцитами и макрофагами [27]. Исследо-вания на мышиных моделях продемонстрировали исключительную роль иммунной системы, а именно субпопуляции CD4+ Т-лимфоцитов в развитии и прогрессировании заболевания [28].…”

Section: роль T-клеточного звена иммунитета в развитии миокардитаunclassified

Immune system in development and progression of viral myocardial damage

Хегай

Trunina

Чеботарева

et al. 2021

Ross. vestn. perinatol. pediatr.

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This review demonstrates the role of the immune system in the development and progression of cardiac pathology caused by viral infection. The authors describe the role of lymphocytes (T- helper-17–Th17) in the viral persistence in myocardial tissue. They provide the information on increased level of interleukin-17A, the main Th17 cytokine in patients with dilated cardiomyopathy, which proves role of these cells in the progression of cardiac pathology. They discuss the role of T regulatory (Treg) lymphocytes in inflammatory heart disease.

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“…Autoantibodies may be produced by an immune response to viral antigens that then cross-react with self-antigens in a process called molecular mimicry. Viruses may also injure myocardial cells and cause them to release self-antigens to which new autoantibodies may form ( 83 ). Antibodies may be made against cell surface antigens as well as intracellular and even intra-mitochondrial antigens ( 79 , 82 ).…”

Section: Clinical Features and Pathophysiology Of Covid-19mentioning

confidence: 99%

“…Viruses may induce an antibody mediated autoimmune process (Type II hypersensitivity). The B cell lineage produce these antibodies and myocarditis animal models point to the considerable impact that B cells and their resultant antibodies have in the pathophysiology (77)(78)(79)(80)(81)(82)(83). Autoantibodies may be produced by an immune response to viral antigens that then cross-react with self-antigens in a process called molecular mimicry.…”

Section: Type II Hypersensitivity In Covid-19mentioning

confidence: 99%

COVID-19: Infection or Autoimmunity

Icenogle¹

2020

Front. Immunol.

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The clinical and laboratory features of COVID-19 are reviewed with attention to the immunologic manifestations of the disease. Recent COVID-19 publications describe a variety of clinical presentations including an asymptomatic state, pneumonia, a hemophagocytic lymphohistiocytosis like syndrome, Multisystem Inflammatory Syndrome in Children (MIS-C) but, also called Pediatric Inflammatory Multisystem Syndrome-Toxic Shock (PIMS-TS), Kawasaki Disease, and myocarditis. A common theme amongst multiple reports suggests an overexuberant autoimmune component of the disease but a common pathophysiology to explain the variations in clinical presentation has been elusive. Review of the basic science of other viral induced autoimmune disorders may give clues as to why immunosuppressive and immunomodulating regimens now appear to have some efficacy in COVID-19. Review of the immunopathology also reveals other therapies that have yet to be explored. There is potential use of T cell depleting therapies and possibly anti-CD20 therapy for COVID-19 and clinical research using these medications is warranted.

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Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy

Cited by 44 publications

References 177 publications

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Immune system in development and progression of viral myocardial damage

COVID-19: Infection or Autoimmunity

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