A humoral and cellular immune response to polysaccharide and protein antigens of the cell wall of streptococci (Groups A, B, C and G) and to homologous myocardial tropomyosin was studied in patients with rheumatoid arthritis (RA) with different clinical variants of disease and in healthy persons. In RA patients humoral and cellular immune reactions to polysaccharide and protein streptococcal antigens were especially marked with the use of the structural components of the cell wall of streptococcus, Group B. Elevated titers of antibodies to homologous myocardial tropomyosin were detected in RA patients as compared to those in a group of healthy persons, an average titer of antibodies to tropomyosin in RA patients with systemic symptoms being much higher than in patients with an articular form of disease. The authors emphasized a possible role of antigens of the cell wall of streptococcus, Group B, in the occurrence and development of immunopathological reactions in RA, and a role of antibodies to myocardial tropomyosin in immunopathogenesis of cardiac disorder in this disease.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Modeling the effects of thin filament near-neighbor cooperative interactions in mammalian myocardium.
J Gen Physiol
March 2025
Department of Animal, Veterinary, and Food Sciences, College of Agricultural and Life Sciences, University of Idaho, Moscow, ID, USA.
The mechanisms underlying cooperative activation and inactivation of myocardial force extend from local, near-neighbor interactions involving troponin-tropomyosin regulatory units (RU) and crossbridges (XB) to more global interactions across the sarcomere. To better understand these mechanisms in the hearts of small and large mammals, we undertook a simplified mathematical approach to assess the contribution of three types of near-neighbor cooperative interactions, i.e.
View Article and Find Full Text PDFHypertrophic cardiomyopathy: insights into pathophysiology and novel therapeutic strategies from clinical studies.
Egypt Heart J
January 2025
Department of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.
Background: Hypertrophic cardiomyopathy (HCM) is a frequently encountered cardiac condition worldwide, often inherited, and characterized by intricate phenotypic and genetic manifestations. The natural progression of HCM is diverse, largely due to mutations in the contractile and relaxation proteins of the heart. These mutations disrupt the normal structure and functioning of the heart muscle, particularly affecting genes that encode proteins involved in the contraction and relaxation of cardiac muscle.
View Article and Find Full Text PDFNovel Mutation Lys30Glu in the Gene Leads to Pediatric Left Ventricular Non-Compaction and Dilated Cardiomyopathy via Impairment of Structural and Functional Properties of Cardiac Tropomyosin.
Int J Mol Sci
December 2024
Research Center of Biotechnology, A.N. Bach Institute of Biochemistry, Russian Academy of Sciences, Moscow 119071, Russia.
Pediatric dilated cardiomyopathy (DCM) is a rare heart muscle disorder leading to the enlargement of all chambers and systolic dysfunction. We identified a novel de novo variant, c.88A>G (p.
View Article and Find Full Text PDFALPK2 prevents cardiac diastolic dysfunction in heart failure with preserved ejection fraction.
FASEB J
November 2024
Department of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
Protein phosphorylation, controlled by protein kinases, is central to regulating various pathophysiological processes, including cardiac systolic function. The dysregulation of protein kinase activity plays a significant role in the pathogenesis of cardiac systolic dysfunction. While cardiac contraction mechanisms are well documented, the mechanisms underlying cardiac diastole remain elusive.
View Article and Find Full Text PDFDilated cardiomyopathy-associated skeletal muscle actin (ACTA1) mutation R256H disrupts actin structure and function and causes cardiomyocyte hypocontractility.
Proc Natl Acad Sci U S A
November 2024
Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110.
Skeletal muscle actin (ACTA1) mutations are a prevalent cause of skeletal myopathies consistent with ACTA1's high expression in skeletal muscle. Rare de novo mutations in ACTA1 associated with combined cardiac and skeletal myopathies have been reported, but ACTA1 represents only ~20% of the total actin pool in cardiomyocytes, making its role in cardiomyopathy controversial. Here we demonstrate how a mutation in an actin isoform expressed at low levels in cardiomyocytes can cause cardiomyopathy by focusing on a unique ACTA1 variant, R256H.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!