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Forsythoside B Ameliorates Neuroinflammation via Inhibiting NLRP3 Inflammasome of Glial Cells in Experimental Autoimmune Encephalomyelitis Mice.
Brain Res Bull
December 2024
Department of Neurology, the First Affiliated Hospital of Hainan Medical University, Haikou 570102, China. Electronic address:
Neuroinflammation mediated by glial cells plays a crucial role in demyelination in experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis (MS) model. Forsythoside B (FTS·B), a natural phenylethanoid glycoside isolated from the dried fruits and leaves of Forsythia suspensa (Thunb.) Vahl, has been found to have antioxidant, anti-apoptotic, and anti-inflammatory properties.
View Article and Find Full Text PDFHyperreactive B cells instruct their elimination by T cells to curb autoinflammation and lymphomagenesis.
Immunity
December 2024
Institute of Experimental Hematology, School of Medicine, Technical University of Munich, 81675 Munich, Germany; Center for Translational Cancer Research (TranslaTUM), School of Medicine, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), 69120 Heidelberg, Germany; Max-Planck Institute of Biochemistry, 82152 Planegg, Germany. Electronic address:
B cell immunity carries the inherent risk of deviating into autoimmunity and malignancy, which are both strongly associated with genetic variants or alterations that increase immune signaling. Here, we investigated the interplay of autoimmunity and lymphoma risk factors centered around the archetypal negative immune regulator TNFAIP3/A20 in mice. Counterintuitively, B cells with moderately elevated sensitivity to stimulation caused fatal autoimmune pathology, while those with high sensitivity did not.
View Article and Find Full Text PDFMRI-based morphometric structural changes correlate with histopathology in experimental autoimmune encephalomyelitis.
J Neurol Sci
December 2024
Institute of Neuroanatomy, Faculty of Medicine, University of Bonn and University Hospital Bonn, Nussallee 10, 53115 Bonn, Germany. Electronic address:
Background And Objectives: Magnetic resonance imaging (MRI) and neurohistopathology are important correlates for evaluation of disease progression in multiple sclerosis (MS). Here we used experimental autoimmune encephalomyelitis (EAE) as an animal model of MS to determine the correlation between clinical EAE severity, MRI and histopathological parameters.
Methods: N = 11 female C57BL/6J mice were immunized with human myelin oligodendrocyte glycoprotein 1-125, while N = 9 remained non-immunized.
Differentiating multiple sclerosis with predominant spinal cord and optic nerve involvement from other autoimmune demyelinating diseases using B cell immunophenotyping and gene expression profiling.
Mult Scler Relat Disord
December 2024
Istanbul University, Aziz Sancar Institute for Experimental Medical Research, Department of Neuroscience, Istanbul, Turkiye.
Objective: Multiple sclerosis (MS) may present with predominant involvement of the spinal cord and optic nerve (MS/w-SCON) and mimic other autoimmune inflammatory demyelinating disorders (AIDD) such as neuromyelitis optica spectrum disorder (NMOSD), and relapsing inflammatory optic neuritis (RION). Thus, biomarkers are required for effective differential diagnosis of AIDD.
Methods: Patients with MS/w-SCON (n = 20), MS without involvement of SCON (MS/wo-SCON) (n = 22), NMOSD (n = 16), RION (n = 15) and healthy individuals (n = 21) were included.
Impact of the clinically approved BTK inhibitors on the conformation of full-length BTK and analysis of the development of BTK resistance mutations in chronic lymphocytic leukemia.
Elife
December 2024
Roy J. Carver Department of Biochemistry, Biophysics and Molecular Biology, Iowa State University, Ames, United States.
Inhibition of Bruton's tyrosine kinase (BTK) has proven to be highly effective in the treatment of B-cell malignancies such as chronic lymphocytic leukemia (CLL), autoimmune disorders, and multiple sclerosis. Since the approval of the first BTK inhibitor (BTKi), Ibrutinib, several other inhibitors including Acalabrutinib, Zanubrutinib, Tirabrutinib, and Pirtobrutinib have been clinically approved. All are covalent active site inhibitors, with the exception of the reversible active site inhibitor Pirtobrutinib.
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