Effects of antibodies obtained from patients with dilated cardiomyopathy on the function of isolated rat hearts

Staudt, Yvonne; Trimpert, Christiane; Birkenmeier, Katrin; Krieg, Thomas; Bemmann, T.; Beug, Daniel; Felix, Stephan B.; Staudt, Alexander

doi:10.1111/j.1365-2362.2006.01603.x

Cited by 8 publications

(8 citation statements)

References 23 publications

(42 reference statements)

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“…Evidence indicates that these autoantibodies affect the heart rather than other organs. Serum or IgG purified from these patients can induce negative inotropic effects on the heart of chicken embryos [53] and decrease heart contraction, the calcium transport [54,55], and the diastolic relaxation in mice [48,56]. The transference of IgG purified from patients serum with cardiac dysfunction to healthy mice induced significant necrosis in cardiomyocytes and mediated inflammatory effects with the aid of immune cells [57].…”

Section: Development Of Cardiac Autoimmunitymentioning

confidence: 99%

IFN-γ versus IL-17: A Battle During Cardiac Autoimmunity Evolution

Kurtenbach¹,

Martinez²

2017

Immunopathogenesis and Immune-Based Therapy for Selected Autoimmune Disorders

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Cardiovascular diseases are the leading global cause of death. Cardiomyopathies are the most prevalent forms of heart failure diseases currently. They may have genetic or environmental etiology, and the development of an autoimmune process is essential for the progression of the disease. During an autoimmune response, there is the breakdown of self-tolerance and generation of a T-lymphocytes-mediated cellular autoimmune response and B-lymphocytes-mediated humoral autoimmune response. Lymphocytes perpetuate the autoimmune response throughout the release of cytokines, expansion of autoreactive clones, and attenuation of regulatory mechanisms. Increasing evidences indicate that interferon (IFN)-γ and interleukin (IL)-17 participate during autoimmune disorders development. The use of autoimmune cardiomyopathy models revealed antagonistic functions for both cytokines during the evolution of autoimmune cardiomyopathy: while enhanced IFN-γ levels are associated to a lower disease severity, the levels of IL-17 are inversely correlated to a favorable prognosis. More precisely, recent findings indicate that the IFN-γ/IL-17 ratio in combination with other cytokine levels dictates heart's autoimmunity development and dilatation. In this chapter, we discuss the role played by the autoimmune response in the development of cardiomyopathy. We also discuss some immune mechanisms focused on IFN-γ and IL-17's ability to induce and perpetuate cardiac autoimmunity.

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Section: Development Of Cardiac Autoimmunitymentioning

confidence: 99%

IFN-γ versus IL-17: A Battle During Cardiac Autoimmunity Evolution

Kurtenbach¹,

Martinez²

2017

Immunopathogenesis and Immune-Based Therapy for Selected Autoimmune Disorders

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“…Further, that group indicated that the anti-cTnI IgG might negatively impact survivability of myocardial ischemia in the mouse model and most recently, has reported that the absence of auto-antibodies against cardiac troponin I predicts improvement of left ventricular function after acute myocardial infarction. 6 Recently, Staudt et al 7 perfused isolated rat hearts with human IgG isolated from DCM patients and suggested that the antibodies impaired contractibility and relaxation and further demonstrated that left ventricular function improved and BNP levels decreased in DCM patients after immunoadsorption (IA) therapy. 8 Thus at present, the presence of autoantibodies may have both an analytical effect on the results from in vitro diagnostic immunoassays for cardiac troponin-I and clinical effects contributing to chronic cardiac diseases like DCM or in acute myocardial infarction.…”

Section: Introductionmentioning

confidence: 99%

Circulating Cardiac Troponin‐I Autoantibodies in Human Plasma and Serum

Adamczyk

Brashear

Mattingly

2009

Annals of the New York Academy of Sciences

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We identified IgG reactive with human cardiac troponin-I (cTnI) in plasma and serum samples (N = 1930) from normal blood donors, and in sample cohorts characterized on the basis of clinical biomarkers associated with cardiac, infectious, and autoimmune diseases. cTnI and brain natriuretic peptide were the biomarkers chosen to reflect myocyte damage or left ventricular dysfunction, respectively. The infectious disease cohorts were serologically positive for antibodies to hepatitis B (natural infection), hepatitis C virus, and Chagas (i.e., T.cruzi). The autoimmune cohorts were represented by samples from diagnosed systemic lupus erythematosus (biomarker: dsDNA) and rheumatoid arthritis (biomarker: rheumatoid factor) subjects. The prevalence of IgG autoantibodies reactive with cTnI was high in the normal donor cohort (95/750, 12.7%). The prevalence in the other sample cohorts was not significantly different from that in the normal blood donors, with the exception of a slight increase in the rheumatoid factor cohort (28/137, 20.4%). The presence of anti-cTnI IgG in highly reactive samples was confirmed by inhibition with the antigen and further by screening with a library of peptides derived from the human cTnI amino acid sequence. Our data suggest that these autoantibodies are polyspecific, encompassing epitopes across the entire cTnI sequence, including the cardiac-specific amino terminal region.

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“…This includes associations of cTn release in experimental models with appearance of cTnAAbs and reduced myocardial contractility; 6 improvements in cardiac function following immunoadsorption in dilated cardiomyopathy, 18 deleterious in vitro systolic and diastolic effects of antibodies isolated from immunoadsorption effluent; 19 and poor functional recovery from acute myocardial infarction in the presence of cTnAAbs. This includes associations of cTn release in experimental models with appearance of cTnAAbs and reduced myocardial contractility; 6 improvements in cardiac function following immunoadsorption in dilated cardiomyopathy, 18 deleterious in vitro systolic and diastolic effects of antibodies isolated from immunoadsorption effluent; 19 and poor functional recovery from acute myocardial infarction in the presence of cTnAAbs.…”

Section: Discussionmentioning

confidence: 99%

“…A small but compelling body of in vitro and clinical evidence supports this hypothesis. This includes associations of cTn release in experimental models with appearance of cTnAAbs and reduced myocardial contractility; 6 improvements in cardiac function following immunoadsorption in dilated cardiomyopathy, 18 deleterious in vitro systolic and diastolic effects of antibodies isolated from immunoadsorption effluent; 19 and poor functional recovery from acute myocardial infarction in the presence of cTnAAbs. 10 The prevalence of cTnAAbs in this HD cohort was of a similar magnitude to previous descriptions (12.9%) from blood donor samples 20 described as "normal" subjects, although American blood donors are likely to significantly under-report comorbidities.…”

Section: Discussionmentioning

confidence: 99%