A5079622093- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Cell Adhesion Molecules Research
- Immune Response and Inflammation
- Sepsis Diagnosis and Treatment
- Immunotherapy and Immune Responses
- CAR-T cell therapy research
- Immune cells in cancer
- Adrenal Hormones and Disorders
- Invertebrate Immune Response Mechanisms
- Immune responses and vaccinations
- Atherosclerosis and Cardiovascular Diseases
- Thermal Regulation in Medicine
- Gut microbiota and health
- Escherichia coli research studies
- NF-κB Signaling Pathways
University of Minnesota
2023-2024
University of Arizona
2022-2024
University of Minnesota Medical Center
2023
Abstract Human sepsis is a complex disease that manifests with diverse range of phenotypes and inherent variability among individuals, making it hard to develop comprehensive animal model. Despite this difficulty, numerous models have been developed capture many key aspects human sepsis. The robustness these vital for conducting pre‐clinical studies test potential therapeutics. In article, we describe four different murine can be used address scientific questions relevant the pathology...
BACKGROUND. Sepsis remains a major clinical challenge for which successful treatment requires greater precision in identifying patients at increased risk of adverse outcomes requiring different therapeutic approaches. Predicting and immunological endotyping septic has generally relied on using blood protein or mRNA biomarkers, static cell phenotyping. Here, we sought to determine whether functional immune responsiveness would yield improved precision.
Uropathogenic
CD4 + T cells use cell receptor (TCR)–CD3 complexes, and CD4, to respond peptide antigens within MHCII molecules (pMHCII). We report here that, through ~435 million years of evolution in jawed vertebrates, purifying selection has shaped motifs the extracellular, transmembrane, intracellular domains eutherian that enhance pMHCII responses, covary with residues an motif inhibits responses. Importantly, while interactions Src kinase, Lck, are viewed as key our data indicate CD4–Lck derive their...
CD4 + T cell activation is driven by 5-module receptor complexes. The (TCR) the module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 coreceptor module. reciprocally TCR-CD3-pMHCII assemblies on outside a cells Src kinase, LCK, inside. Previously, we reported transmembrane GGXXG cytoplasmic juxtamembrane (C/F)CV+C motifs found in eutherian (placental mammal) have...
CD4 + T cell activation is driven by five-module receptor complexes. The (TCR) the module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 coreceptor module. reciprocally TCR-CD3-pMHCII assemblies on outside a cells Src kinase, LCK, inside. Previously, we reported transmembrane GGXXG cytoplasmic juxtamembrane (C/F)CV+C motifs found in eutherian (placental mammal)...
Bacterial infections are the primary cause of pathogenic sepsis. An uropathogenic E. coli (UPEC) model monomicrobial sepsis represents a useful tool for interrogating host immune response to this pathogen. Here, we present protocol inducing in mice using UPEC. We describe steps preparing bacteria, delivering UPEC into mice, and monitoring post-infection. then detail procedures measuring cytokine detecting cell subsets flow cytometry. For complete details on use execution protocol, please...
CD4 + T cell activation is driven by five-module receptor complexes. The (TCR) the module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 coreceptor module. reciprocally TCR-CD3-pMHCII assemblies on outside a cells Src kinase, LCK, inside. Previously, we reported transmembrane GGXXG cytoplasmic juxtamembrane (C/F)CV+C motifs found in eutherian (placental mammal)...
CD4 + T cell activation is driven by 5-module receptor complexes. The (TCR) the module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 coreceptor module. reciprocally TCR-CD3-pMHCII assemblies on outside a cells Src kinase, Lck, inside. Previously, we reported transmembrane GGXXG motif cytoplasmic juxtamembrane (C/F)CV+C found in eutherian (placental mammals) have...
Abstract CD4 + T cell activation is driven by 5-module receptor complexes. The (TCR) the module that binds composite surfaces of peptide antigens embedded within MHCII molecules (pMHCII). It associates with three signaling modules (CD3γε, CD3δε, and CD3ζζ) to form TCR-CD3 coreceptor module. reciprocally TCR-CD3-pMHCII assemblies on outside a cells Src kinase, LCK, inside. Previously, we reported transmembrane GGXXG cytoplasmic juxtamembrane (C/F)CV+C motifs found in eutherian (placental...
Abstract T-cells play a central role in adaptive immunity by recognizing peptide-antigens presented MHC molecules (pMHC) via their clonotypic T-cell receptors (TCRs). αβTCRs are heterodimers, consisting of TCRα and TCRβ subunits that composed variable (Vα, Vβ) constant (Cα, Cβ) domains. While the Vα, Vβ, Cβ domains adopt typical immunoglobulin (Ig) folds extracellular space, Cα domain lacks top β sheet instead has two loosely associated strands (C F strands) on its surface. Previous results...
T cells play a central role in adaptive immunity by recognizing peptide Ags presented MHC molecules (pMHC) via their clonotypic TCRs. αβTCRs are heterodimers, consisting of TCRα and TCRβ subunits that composed variable (Vα, Vβ) constant (Cα, Cβ) domains. Whereas the Vα, Vβ, Cβ domains adopt typical Ig folds extracellular space, Cα domain lacks top β sheet instead has two loosely associated strands (C- F-strands) on its surface. Previous results suggest this unique Ig-like fold mediates...