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γδ T Cells in Epithelial Surveillance and Inflammation: Insights from Organoid Models and Multimodal Analysis

By SWA
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Introduction γδ T cells are a unique subset of T lymphocytes characterized by their expression of a gamma-delta (γδ) T-cell receptor (TCR), in contrast to the conventional alpha-beta (αβ) TCR found on most T cells. Unlike αβ T cells, which are central to adaptive immunity and rely on antigen presentation by MHC molecules, γδ T cells exhibit innate-like properties, responding rapidly to stress signals and microbial patterns without requiring classical antigen presentation. A particularly important aspect of γδ T cell biology is their close interaction with epithelial cells at barrier sites, such as the skin , gastrointestinal tract , respiratory epithelium , and urogenital tract . These cells play a crucial role in epithelial homeostasis, tissue repair , and the regulation of inflammation . Recent advances in organoid technology have provided a physiologically relevant platform to investigate the behavior and function of γδ T cells in controlled three-dimensional (3D) epithelial env...
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Understanding JAK Inhibitors and NSAIDs: Mechanisms, Uses, and Testing Possibilities with Genetic Marker GS191

By SWA
JAK inhibitors and nonsteroidal anti-inflammatory drugs (NSAIDs) are both critical tools in the management of inflammation and autoimmune diseases. Although they share the common goal of reducing inflammation, they operate through entirely different biological mechanisms. This distinction allows for tailored treatment strategies, especially in complex, chronic inflammatory conditions like ankylosing spondylitis or rheumatoid arthritis. How They Work JAK Inhibitors JAK inhibitors target the Janus Kinase (JAK) family of enzymes. These enzymes play a central role in the JAK-STAT signaling pathway , which is crucial in mediating immune responses and inflammation. When this pathway is overactive, as in many autoimmune diseases, JAK inhibitors can help reduce the excessive immune response and inflammation by blocking intracellular signals that promote cytokine production. NSAIDs NSAIDs—such as ibuprofen, naproxen, and celecoxib—work by inhibiting cyclooxygenase (COX) enzymes, partic...
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NSAIDs – Impaired Metabolism (GS191 Genetic Marker)

By SWA
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Summary The GS191 genetic marker is associated with impaired metabolism of NSAIDs (non-steroidal anti-inflammatory drugs), potentially leading to increased toxicity or reduced clearance of these drugs. If this marker is present, NSAID use should be approached with caution or avoided, depending on the specific drug and the patient’s overall clinical context. What is GS191? The GS191 marker is a pharmacogenetic variant identified in certain genetic screening platforms, such as GeneSight and other pharmacogenomic tests. It is not a standard single nucleotide polymorphism (SNP) identifier like rs1057910 but is more likely a proprietary label used to summarize one or more relevant variants—particularly those that impact the metabolism of NSAIDs. This marker typically reflects altered function in cytochrome P450 enzymes, especially: CYP2C9 , the primary enzyme responsible for metabolizing many NSAIDs including ibuprofen, diclofenac, and celecoxib. CYP2C8 and CYP3A4 , which also cont...
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