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Increased Inflammation as well as Decreased Endoplasmic Reticulum Stress and Translation Differentiate Pancreatic Islets of Pre-symptomatic Stage 1 Type 1 Diabetes and Non-diabetic Cases.
bioRxiv
September 2024
Integrative Omics, Biological Sciences Division, Pacific Northwest National Laboratory, Richland, WA.
Article Synopsis
- This study investigates the molecular changes in insulin-secreting β-cells in individuals at the pre-symptomatic stage of type 1 diabetes (T1D) to better understand how the disease progresses.
- * Researchers used a proteomics approach to analyze islet sections from organ donors with islet autoantibodies, comparing them to nondiabetic controls to identify potential markers of β-cell dysfunction.
- * The analysis revealed about 202 proteins with significant differences between high-risk autoantibody-positive cases and controls, highlighting changes related to immune response, glycolysis, and decreased levels of endoplasmic reticulum stress response and protein synthesis.
The atypical chemokine receptor 2 reduces T cell expansion and tertiary lymphoid tissue but does not limit autoimmune organ injury in lupus-prone B6lpr mice.
Front Immunol
May 2024
Division of Nephrology, Department of Medicine IV, LMU University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany.
Introduction: The atypical chemokine receptor 2 (ACKR2) is a chemokine scavenger receptor, which limits inflammation and organ damage in several experimental disease models including kidney diseases. However, potential roles of ACKR2 in reducing inflammation and tissue injury in autoimmune disorders like systemic lupus erythematosus (SLE) and lupus nephritis are unknown, as well as its effects on systemic autoimmunity.
Methods: To characterize functional roles of ACKR2 in SLE, genetic Ackr2 deficiency was introduced into lupus-prone C57BL/6lpr (Ackr2-/- B6lpr) mice.
Desmosomal 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 PDFCollage of cases and brief review of the laboratory diagnosis and molecular testing in autoimmune haemolytic anaemia.
J Family Med Prim Care
February 2024
Department of Pathology, Saraswati Institute of Medical Sciences, Hapur, Uttar Pradesh, India.
Autoimmune haemolytic anaemia (AIHA) is an acquired heterogenous clinical entity with variable presentations like acute haemolysis or mild, chronic haemolysis compounded with acute exacerbation in winters or fatal uncompensated haemolysis. A step-wise approach to the diagnosis and characterisation of AIHA should be undertaken, firstly the diagnosis of haemolysis followed by the establishment of immune nature with the aid of direct agglutination tests (DAT). Simultaneously the other causes of immune haemolysis need to be excluded too.
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