Publications by authors named "R E Brink"
The unexplained association between infection and autoimmune disease is strongest for hepatitis C virus-induced cryoglobulinemic vasculitis (HCV-cryovas). To analyze its origins, we traced the evolution of pathogenic rheumatoid factor (RF) autoantibodies in four HCV-cryovas patients by deep single-cell multi-omic analysis, revealing three sources of B cell somatic mutation converged to drive the accumulation of a large disease-causing clone. A method for quantifying low-affinity binding revealed recurring antibody variable domain combinations created by V(D)J recombination that bound self-immunoglobulin G (IgG) but not viral E2 antigen.
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- Children learn about art by interacting with their environment, making museums valuable for their development.
- The study uses mobile eye tracking at the Rijksmuseum to see how child-friendly painting descriptions affect their viewing behavior.
- Results indicate that tailored information helps children focus longer on important details, while adult-oriented descriptions do not engage them effectively.
Existing antibodies (Abs) have varied effects on humoral immunity during subsequent infections. Here, we leveraged in vivo systems that allow precise control of antigen-specific Abs and B cells to examine the impact of Ab dose, affinity, and specificity in directing B cell activation and differentiation. Abs competing with the B cell receptor (BCR) epitope showed affinity-dependent suppression.
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- Researchers studied mutations in a gene that affects a key protein involved in cell signaling, which is linked to severe health issues like impaired immunity in patients.
- The mutations were found to disrupt normal cell behavior by promoting excessive cell growth and responses to immune signals, specifically T cell receptor stimulation.
- The mutant protein was shown to interfere with a regulatory protein, leading to heightened activity of important signaling pathways that contribute to cell growth and survival.
Acute kidney injury (AKI) disrupts energy metabolism. Targeting metabolism through AMP-activated protein kinase (AMPK) may alleviate AKI. ATX-304, a pan-AMPK activator, was evaluated in C57Bl/6 mice and tubular epithelial cell (TEC) cultures.
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