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Unraveling calcium dysregulation and autoimmunity in immune mediated rippling muscle disease.
Acta Neuropathol Commun
January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, 55905, USA.
Rippling Muscle Disease (RMD) is a rare skeletal myopathy characterized by abnormal muscular excitability manifesting with wave-like muscle contractions and percussion-induced muscle mounding. Hereditary RMD is associated with caveolin-3 or cavin-1 mutations. Recently, we identified cavin 4 autoantibodies as a biomarker of immune-mediated RMD (iRMD), though the underlying disease-mechanisms remain poorly understood.
View Article and Find Full Text PDFAutoantibodies immuno-mechanically modulate platelet contractile force and bleeding risk.
Nat Commun
November 2024
The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Altered mechanotransduction has been proposed as a putative mechanism for disease pathophysiology, yet evidence remains scarce. Here we introduce a concept we call single cell immuno-mechanical modulation, which links immunology, integrin biology, cellular mechanics, and disease pathophysiology and symptomology. Using a micropatterned hydrogel-laden coverslip compatible with standard fluorescence microscopy, we conduct a clinical mechanobiology study, specifically focusing on immune thrombocytopenia (ITP), an autoantibody-mediated platelet disorder that currently lacks a reliable biomarker for bleeding risk.
View Article and Find Full Text PDFDesmosomal Cadherin Tension Loss in Pemphigus Vulgaris Mediated by the Inhibition of Active RhoA at Cell-Cell Adhesions.
bioRxiv
May 2024
Department of Mechanical and Materials Engineering, University of Nebraska-Lincoln, Lincoln, NE 68588.
Binding of autoantibodies to keratinocyte surface antigens, primarily desmoglein 3 (Dsg3) of the desmosomal complex, leads to the dissociation of cell-cell adhesion in the blistering disorder pemphigus vulgaris (PV). After the initial disassembly of desmosomes, cell-cell adhesions actively remodel in association with the cytoskeleton and focal adhesions. Growing evidence highlights the role of adhesion mechanics and mechanotransduction at cell-cell adhesions in this remodeling process, as their active participation may direct autoimmune pathogenicity.
View Article and Find Full Text PDFChange of voltage-gated sodium channel repertoire in skeletal muscle of a MuSK myasthenia gravis mouse model.
Eur J Neurosci
June 2024
Department of Neurology, Leiden University Medical Center, Leiden, The Netherlands.
Muscle-specific kinase myasthenia gravis (MuSK MG) is caused by autoantibodies against MuSK in the neuromuscular junction (NMJ). MuSK MG patients have fluctuating, fatigable skeletal muscle weakness, in particular of bulbar muscles. Severity differs greatly between patients, in spite of comparable autoantibody levels.
View Article and Find Full Text PDFAltered serum levels of cytokines in patients with myasthenia gravis.
Heliyon
January 2024
Department of Neurology, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, PR China.
Article Synopsis
- Myasthenia gravis (MG) is an autoimmune disease that causes muscle weakness due to autoantibodies; this study examined the link between cytokines and various aspects of MG such as type, disease progression, and comorbidities.
- Levels of the cytokine IL-6 were found to be significantly higher in MG patients compared to healthy individuals and were especially elevated in those with generalized MG versus ocular MG.
- The study also showed that certain cytokine levels, such as IL-2, were lower in patients with late-onset MG and those with comorbid conditions like diabetes, indicating that these factors may influence cytokine profiles in MG.
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