Neutralization of IL-17 inhibits the production of anti-ANT autoantibodies in CVB3-induced acute viral myocarditis

Yuan, Jing; Yu, Miao; Lin, Qiong-Wen; Cao, Axiu; Lei, Yu; Dong, Jing; Wang, Jinping; Zhang, Jinghui; Wang, Min; Guo, Hao; Liao, Yuhua

doi:10.1016/j.intimp.2009.11.010

Cited by 46 publications

(32 citation statements)

References 30 publications

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“…Besides the proinflammatory effect of Th17 cells, our earlier research suggested that Th17 cells could facilitate the production of autoantibodies in the development of AVMC (5,6). However, the relationship between Th17 cells and CVB3 replication remains unknown in AVMC.…”

mentioning

confidence: 97%

Th17 Cells Contribute to Viral Replication in Coxsackievirus B3-Induced Acute Viral Myocarditis

Yuan¹,

Yu²,

Lin³

et al. 2010

The Journal of Immunology

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Acute viral myocarditis (AVMC) is characterized by virus-triggered myocardial inflammation, and Coxsackievirus B3 (CVB3) is the primary pathogen. We previously proved that Th17 cells, besides having proinflammatory effects, were involved in AVMC by enhancing humoral response. However, the relationship between Th17 cells and CVB3 replication remains unknown. In this experiment, we infected BALB/c mice with CVB3 for establishing AVMC models and then found that, with the increase of viral replication, the expressions of splenic Th17 cells, serum IL-17, and cardiac IL-17 mRNA were elevated significantly, accompanied by the progressive cardiac injuries of AVMC. Furthermore, on day 5, the peak time for viral replication, correlation was positive between cardiac IL-17 mRNA and CVB3 RNA (correlation index = 0.835; p < 0.01). Although the expressions of Th1 and CD8+ T cells, which could secrete the antiviral cytokine IFN-γ and damage the heart, were also elevated, along with Th17 cells, in AVMC, the neutralization of IL-17 further upregulated the percentages of splenic Th1 and CD8+ T cells and the levels of cardiac IFN-γ mRNA. The cardiac pathological changes were obviously improved after neutralization, with reduced viral replication followed by decreases in the cardiac inflammatory cytokines IL-17, TNF-α, and IL-1β. These data suggest that Th17 cells contribute to CVB3 replication in AVMC, and that IL-17 might be an important target for regulating the balance of antiviral immunities.

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mentioning

confidence: 97%

Th17 Cells Contribute to Viral Replication in Coxsackievirus B3-Induced Acute Viral Myocarditis

Yuan¹,

Yu²,

Lin³

et al. 2010

The Journal of Immunology

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“…It is hypothesized that the protective effect of IL-17 inhibition on cardiac inflammation is due to inhibition of CD19(ϩ) B-lymphocyte proliferation and reduction of secretion of anti-ANT autoantibodies by these cells. 60 …”

Section: Antimitochondrial Autoantibodiesmentioning

confidence: 99%

Autoantibodies in Heart Failure and Cardiac Dysfunction

Kaya

Leib

Katus

2012

Circulation Research

158

151

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Abstract:Human heart failure is a disease with multifactorial causes, considerable morbidity, and high mortality.Several circulating autoantibodies, some of them being heart-specific, play a crucial role in the progression and induction of heart failure. However the precise mechanisms on how these autoantibodies perpetuate or even induce an organ specific autoimmune response are not yet fully understood. Also it is being a matter of current research to elucidate a potential pathophysiological role of the innate immune system in generating auto-reactive antibodies. In this review we will summarize the current available literature on circulating autoantibodies which are related to human heart failure. We will present clinical and animal studies that demonstrate the occurrence and pathophysiological relevance of several autoantibodies in heart failure, as well as point out biological mechanisms on molecular and cellular level. Finally the beneficial therapeutic effects of numerous clinical studies that target the humoral arm of the immune system by using either intravenous immunoglobulins and/or immunoadsorption will be critically discussed. (Circ Res. 2012;110:145-158.)

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“…Recently, some studies (Harrington et al, 2005;Steinman, 2007;Korn et al, 2009;Miossec, 2009;Yuan et al, 2010a;2010c) pointed out that IL-17, widely known as a Th17-derived proinflammatory cytokine, may serve as a vital function for inflammatory and autoimmunity diseases, which further supports the concept of IL-17 being targeted for treatment. Using IL-17 McAb-treated VMC mice, Fan et al (2011) found that neutralizing IL-17 with anti-IL-17 can improve myocarditis manifestation and retard the diseases course.…”

Section: Liaomentioning

confidence: 98%

Advances in monoclonal antibody application in myocarditis

Han

Wang

et al. 2013

J. Zhejiang Univ. Sci. B

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Abstract:Monoclonal antibodies have become a part of daily preparation technologies in many laboratories. Attempts have been made to apply monoclonal antibodies to open a new train of thought for clinical treatments of autoimmune diseases, inflammatory diseases, cancer, and other immune-associated diseases. This paper is a prospective review to anticipate that monoclonal antibody application in the treatment of myocarditis, an inflammatory disease of the heart, could be a novel approach in the future. In order to better understand the current state of the art in monoclonal antibody techniques and advance applications in myocarditis, we, through a significant amount of literature research both domestic and abroad, developed a systematic elaboration of monoclonal antibodies, pathogenesis of myocarditis, and application of monoclonal antibodies in myocarditis. This paper presents review of the literature of some therapeutic aspects of monoclonal antibodies in myocarditis and dilated cardiomyopathy to demonstrate the advance of monoclonal antibody application in myocarditis and a strong anticipation that monoclonal antibody application may supply an effective therapeutic approach to relieve the severity of myocarditis in the future. Under conventional therapy, myocarditis is typically associated with congestive heart failure as a progressive outcome, indicating the need for alternative therapeutic strategies to improve long-term results. Reviewing some therapeutic aspects of monoclonal antibodies in myocarditis, we recently found that monoclonal antibodies with high purity and strong specificity can accurately act on target and achieve definite progress in the treatment of viral myocarditis in rat model and may meet the need above. However, several issues remain. The technology on how to make a higher homologous and weak immunogenic humanized or human source antibody and the treatment mechanism of monoclonal antibodies may provide solutions for these open issues. If we are to further stimulate progress in the area of clinical decision support, we must continue to develop and refine our understanding and use of monoclonal antibodies in myocarditis.

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Neutralization of IL-17 inhibits the production of anti-ANT autoantibodies in CVB3-induced acute viral myocarditis

Cited by 46 publications

References 30 publications

Th17 Cells Contribute to Viral Replication in Coxsackievirus B3-Induced Acute Viral Myocarditis

Th17 Cells Contribute to Viral Replication in Coxsackievirus B3-Induced Acute Viral Myocarditis

Autoantibodies in Heart Failure and Cardiac Dysfunction

Advances in monoclonal antibody application in myocarditis

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