A5053818687- Immune Cell Function and Interaction
- Inflammasome and immune disorders
- IL-33, ST2, and ILC Pathways
- Immune cells in cancer
- Immunotherapy and Immune Responses
- Phagocytosis and Immune Regulation
- interferon and immune responses
- T-cell and B-cell Immunology
- Enzyme Catalysis and Immobilization
- RNA regulation and disease
- Cytokine Signaling Pathways and Interactions
- Epigenetics and DNA Methylation
- Viral Infections and Vectors
- Enzyme Production and Characterization
- Microbial Metabolites in Food Biotechnology
Cincinnati Children's Hospital Medical Center
2018-2020
The University of Texas Southwestern Medical Center
2017-2020
Significance Macrophages initiate inflammation to eliminate invading microbes. Following clearance of inflammatory stimuli, macrophages down-regulate genes and express repair protect host tissues from damage. Here, we find that the adaptor B-cell adapter for PI3K (BCAP) facilitates this transition reparative macrophages. Absence BCAP in limits ability mice intestinal following Toll-like receptor stimulation, undergo aerobic glycolysis results lactate production, a process compromised...
Patients with stimulator of interferon genes (STING)-associated vasculopathy onset in infancy (SAVI) develop systemic inflammation characterized by vasculopathy, interstitial lung disease, ulcerative skin lesions, and premature death. Autosomal dominant mutations STING are thought to trigger activation IRF3 subsequent up-regulation (IFN)-stimulated (ISGs) patients SAVI. We generated heterozygous N153S knock-in mice as a model These spontaneously developed within the lung, hypercytokinemia, T...
Signal regulatory protein (SIRPα) is an immune inhibitory receptor expressed by myeloid cells to inhibit cell phagocytosis, migration, and activation. Despite the progress of SIRPα CD47 antagonist antibodies promote anti-cancer immunity, it not yet known whether agonism could restrain excessive autoimmune tissue inflammation. Here, we report that neutrophil- monocyte-associated genes including SIRPA are increased in inflamed biopsies from patients with rheumatoid arthritis inflammatory bowel...
Dendritic cells (DCs) are critical for the differentiation of pathogen-specific CD4 T cells. However, to what extent innate cues from DCs dictate transcriptional changes in remains elusive. Here, we used stimulated with specific pathogens prime vitro and found that these express unique profiles dictated by nature priming pathogen. More specifically, transcriptome C. rodentium-primed Th17 resembled primed following infection vivo but was remarkably distinct cytokine-polarized We identified...
We report the heterologous expression and molecular characterization of first extremely halophilic alpha-glucosidase (EC 3.2.1.20) from archaeon Haloquadratum walsbyi. A 2349 bp region (Hqrw_2071) Hqr. walsbyi C23 annotated genome was PCR-amplified resulting amplicon ligated into plasmid pET28b(+), expressed in E. coli Rosetta cells, protein purified by Ni-NTA affinity chromatography. The recombinant showed an estimated mass 87 kDa, consistent with expected value protein, optimal activity...
Abstract While IL-1β is critical for anti-microbial host defense, it also a key mediator of autoimmune inflammation. Inflammasome activation following pathogenic insults known to result in production. However, the molecular events that produce during T cell driven diseases remain unclear. Here, we have discovered an inflammasome-independent pathway production triggered upon cognate interactions between dendritic cells and effector CD4 cells. Analogous inflammasome activation, this “T...
One sentence summary Our study revealed that DCs shape distinct pathogen-specific CD4 T cell transcriptome and from which, we discovered an unexpected role for T-cell-intrinsic caspase-1 in promoting Th17 differentiation. ABSTRACT Dendritic cells (DCs) are critical priming differentiation of cells. However, to what extent innate cues dictate transcriptional changes leading effector heterogeneity remains elusive. Here have used vitro approach prime naïve by stimulated with pathogens. We found...