Publications by authors named "Eugene Rudensky"
Article Synopsis
- * Intraepithelial lymphocytes (IELs), particularly those with γ and δ T cell receptors, play a potential role in protecting Paneth cells that are vulnerable due to the ATG16L1 gene associated with Crohn's disease.
- * The study identifies apoptosis inhibitor 5 (API5) as a protective factor secreted by γδ IELs, which helps maintain Paneth cell viability, suggesting that API5 could be a therapeutic target to counteract genetic susceptibility in the context of intestinal inflammation.
Humoral immunity in mammals relies on the function of two developmentally and functionally distinct B-cell subsets-B1 and B2 cells. While B2 cells are responsible for the adaptive response to environmental antigens, B1 cells regulate the production of polyreactive and low-affinity antibodies for innate humoral immunity. The molecular mechanism of B-cell specification into different subsets is understudied.
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- The study aims to enhance precision medicine by utilizing patient-derived materials to predict disease progression and treatment outcomes, particularly focusing on intestinal graft-versus-host disease (GVHD).
- Researchers created an ex vivo platform using mouse models to understand the genetic factors, specifically the Atg16L1 gene, that influence susceptibility to T-cell-mediated damage in GVHD.
- The findings suggest that inhibiting necroptosis or interferon signaling can protect human organoids with the Atg16L1 variant from T-cell attacks, offering a potential strategy for individualized therapeutic interventions.
As a conserved pathway that lies at the intersection between host defence and cellular homeostasis, autophagy serves as a rheostat for immune reactions. In particular, autophagy suppresses excess type I interferon (IFN-I) production in response to viral nucleic acids. It is unknown how this function of autophagy relates to the intestinal barrier where host-microbe interactions are pervasive and perpetual.
View Article and Find Full Text PDFProtein lysine methylation is one of the most widespread post-translational modifications in the nuclei of eukaryotic cells. Methylated lysines on histones and nonhistone proteins promote the formation of protein complexes that control gene expression and DNA replication and repair. In the cytoplasm, however, the role of lysine methylation in protein complex formation is not well established.
View Article and Find Full Text PDFEpigenetic gene silencing in eukaryotes is regulated in part by lysine methylation of the core histone proteins. While histone lysine methylation is known to control gene expression through the recruitment of modification-specific effector proteins, it remains unknown whether nonhistone chromatin proteins are targets for similar modification-recognition systems. Here we show that the histone H3 methyltransferase G9a contains a conserved methylation motif with marked sequence similarity to H3 itself.
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