Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy

Maisch, Bernhard; Deeg, P; Liebau, G.; Kochsiek, K

doi:10.1016/0002-9149(83)90535-0

Cited by 186 publications

(58 citation statements)

References 27 publications

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“…2,3 Although chronic viral infection has long been recognized as a candidate causative factor for these pathophysiological mechanisms, 3 a number of experimental models have demonstrated the crucial role 4,5 of myocardial structure-mediated autoimmune processes, which follow the myocardial damage provoked by the initial viral infection. 6,7 The presence of autoantibodies against myocardial structure in patients with myocarditis and dilated cardiomyopathy 8,9 supports the involvement of myocardial structure-mediated autoimmune processes in these settings in humans.…”

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confidence: 95%

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

et al. 2006

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Background-The therapeutic potential of ␤2-adrenergic receptor (AR) agonists in the treatment of autoimmune diseases has been reported. However, the role of these drugs in the myocardial structure-induced autoimmune process, which is thought to play a crucial role in the progression of myocarditis to subsequent complications, has not been elucidated. Methods and Results-Experimental autoimmune myocarditis (EAM) was induced in rats by immunization with cardiac myosin. On daily administration from day 0 after immunization, the ␤2-selective AR agonists formoterol or salbutamol ameliorated EAM on day 21 and increased myocardial interleukin-10/interferon-␥ mRNA levels. Propranolol, a nonselective ␤-AR antagonist, aggravated EAM on day 21 and decreased mRNA levels, whereas metoprolol, a ␤1-selective AR antagonist, showed no effect. These results were reflected in vivo by the proliferation of cardiac myosin-primed lymph node cells from drug-treated rats. In vitro addition of ␤2-selective AR agonists inhibited the activation of cardiac myosin fragment-specific myocarditogenic T lymphocytes, and this effect was reversed by ICI118,551, a ␤2-selective AR antagonist. Furthermore, treatment with 2 different ␤2-selective AR agonists starting on day 14 also ameliorated EAM on day 21. Conclusions-␤2-AR

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confidence: 95%

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

et al. 2006

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“…Myocarditis is an inflammatory disease of the heart and a precursor of dilated cardiomyopathy (Woodruff, 1980;Maisch et al, 1982;1983;Aretz, 1987;Aretz et al, 1987;Brown and O'Connell, 1995;Caforio et al, 1996;Felker et al, 1999). Myocarditis is often characterized by a cellular infiltrate, and if inflammation of the myocardium does not resolve at the acute stage, the heart may be compromised due to necrosis and direct loss of myocytes (Huber et al, 1980), injury from granulomatous inflammation (Cooper et al, 1997;Cooper, 2000), or fibrosis due to proliferation of fibroblasts and collagen deposition (Fairweather et al, 2004;, which can lead to dilated myocardiopathy and ultimately to congestive heart failure (Cooper, 2009).…”

Section: Etiology and Pathogenesis Of Autoimmune Myocarditismentioning

confidence: 99%

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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“…Evidence for cellular autoimmunity in clinical disease is more difficult to obtain. Abnormal helper and suppressor T-lymphocyte numbers are observed during myocarditis (3,26,34,122), and T lymphocytes derived from biopsy specimens show significant reactivity to cardiac antigens in culture (75,88,89).…”

Section: Autoimmunity In Myocarditismentioning

confidence: 99%

Clinical and experimental aspects of viral myocarditis

et al. 1989

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Picornaviruses are frequently implicated as the etiological agents of acute myocarditis. This association is based historically on serological evidence of rising antibody titers to specific pathogens and more recently on identification of viral genomic material in endocardial biopsy specimens through in situ hybridization. Only rarely is infectious virus isolated from either the patient or the heart during periods of maximum myocardial inflammation and injury. Thus, despite a probable viral etiology, much interest centers on the role of the immune system in cardiac damage and the likelihood that the infection triggers an autoimmune response to heart-specific antigens. Heart-reactive antibodies and T cells are found in most myocarditis patients, and immunosuppressive therapy has proven beneficial in many, though not all, cases. Furthermore, murine models of coxsackievirus group B type 3-induced myocarditis also demonstrate that virus infection initiates autoimmunity and that these autoimmune effectors are predominately responsible for tissue injury. How virus-host interactions overcome presumed self-tolerance to heart antigens is discussed, and evidence supporting various theories of virus-initiated autoimmunity and disease pathogenesis are delineated.

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Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy

Cited by 186 publications

References 27 publications

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

β2-Adrenergic Agonists Suppress Rat Autoimmune Myocarditis

Advances in monoclonal antibody application in myocarditis

Clinical and experimental aspects of viral myocarditis

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