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Systemic lupus erythematosus and pulmonary tuberculosis in a patient developing acute-onset type 1 diabetes.
Diabetol Int
January 2025
Department of Endocrinology and Diabetes, NTT Medical Center Tokyo, 141-86255-9-22 Higashi-Gotanda, Shinagawa-ku, Tokyo Japan.
A 73-year-old Japanese woman was admitted to our hospital with anorexia, weight loss, and fever. A few weeks prior to admission, she became aware of anorexia. She was leukopenic, complement-depleted, and positive for antinuclear antibodies and anti-double stranded DNA antibodies.
View Article and Find Full Text PDFUnlabelled: The complement cascade is a front-line defense against pathogens. Complement activation generates the membrane attack complex (MAC), a 10-11 nm diameter pore formed by complement proteins C5b through C8 and polymerized C9. The MAC embeds within the outer membrane of Gram-negative bacteria and displays bactericidal activity.
View Article and Find Full Text PDFNonapoptotic caspase-3 guides C1q-dependent synaptic phagocytosis by microglia.
Nat Commun
January 2025
Department of Translational Neurobiology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, 187-8502, Japan.
Caspases are known to mediate neuronal apoptosis during brain development. However, here we show that nonapoptotic activation of caspase-3 at presynapses drives microglial synaptic phagocytosis. Real-time observation and spatiotemporal manipulation of synaptic caspase-3 in the newly established, mouse-derived culture system demonstrate that increased neuronal activity triggers localized presynaptic caspase-3 activation, facilitating synaptic tagging by complements.
View Article and Find Full Text PDFClinical ischemia-reperfusion injury: Driven by reductive rather than oxidative stress? A narrative review.
Biochim Biophys Acta Bioenerg
January 2025
Department of Surgery and Leiden Transplant Center, Leiden University Medical Center, Leiden, the Netherlands. Electronic address:
Ischemia-reperfusion (IR) injury remains a major contributor to organ dysfunction following transient ischemic insults. Although numerous interventions have been found effective to reduce IR injury in preclinical models, none of these therapies have been successfully translated to the clinical setting. In the context of the persistent translational gap, we systematically investigated the mechanisms implicated in IR injury using kidney donation and transplantation as a clinical model of IR.
View Article and Find Full Text PDFOpportunities and limitations of B cell depletion approaches in SLE.
Nat Rev Rheumatol
February 2025
Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.
B cell depletion with rituximab, a chimeric monoclonal antibody that selectively targets B cells by binding CD20, has been used off label in severe and resistant systemic lupus erythematosus (SLE) for over two decades. Several biological mechanisms limit the efficacy of rituximab, including immunological reactions towards the chimeric molecule, increased numbers of residual B cells, including plasmablasts and plasma cells, and a post-treatment surge in B cell-activating factor (BAFF) levels. Consequently, rituximab induces remission in only a proportion of patients, and safety issues limit its use.
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