Publications by authors named "John J Kaminski"
Article Synopsis
- Synthetic oligodeoxynucleotides (ODNs) with the TTAGGG motif inhibit TLR9 signaling, leading to reduced inflammatory responses, phosphorylation of STAT1 and STAT4, and activation of immune pathways.
- The study found that ODN-A151 prevents the activation of dendritic cells and macrophages in response to cytosolic double-stranded DNA (dsDNA), blocking the production of key inflammatory cytokines.
- A151's effectiveness relies on its unique phosphorothioate backbone and its ability to bind to AIM2, preventing the formation of the AIM2 inflammasome complex, thus offering potential for treating infectious and autoimmune diseases.
The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell surface or within distinct intracellular compartments. These include the Toll-like receptors (TLRs), the retinoic acid-inducble gene I-like receptors (RLRs), the nucleotide oligomerization domain-like receptors (NLRs, also called NACHT, LRR and PYD domain proteins) and cytosolic DNA sensors.
View Article and Find Full Text PDFBackground: When challenged with extracellular fluid shear stress, vascular endothelial cells are known to release nitric oxide, an important vasodilator. Here, we show that the ability of cultured endothelial cells to sense a low range of fluid shear depends on apical membrane organelles, called cilia, and that cilia are compartments required for proper localization and function of the mechanosensitive polycystin-1 molecule.
Methods And Results: Cells with the Pkd1(null/null) or Tg737(orpk/orpk) mutation encoded for polycystin-1 or polaris, respectively, are unable to transmit extracellular shear stress into intracellular calcium signaling and biochemical nitric oxide synthesis.