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Metabolic drivers of PPAR-gamma activity in human CD4 T cells (ongoing). CD4 T cells are required for host defense against microorganisms but also contribute to chronic inflammatory diseases. Following their activation, CD4 T cells differentiate into subsets named Th1, Th2, Th9, Th17 and regulatory T cells (Tregs). This is associated with metabolic changes that result in aerobic glycolysis being utilized for ATP synthesis rather than oxidative phosphorylation. Whereas different T cell subsets have been assessed for their metabolic characteristics following activation, extrinsic factors that shape T cell immunity by modifying cellular metabolism are not well studied. PPAR-g is a master regulator of lipid metabolism and also has anti-inflammatory functions. Previous studies found roles for PPAR-g in regulating CD4 T cell function; however, the metabolic drivers of PPAR-g expression and function have not been elucidated. This study will identify metabolic requirements for PPAR-g expression during human CD4 T cell differentiation, and also investigate how PPAR-g regulates T cell metabolism. Results are expected to help to close the gap in our understanding of how metabolic switches influence the outcome of immune responses. Overall, defining the mechanisms that link metabolism to T cell activation may provide novel therapeutic targets for inflammatory diseases.
Exploring the role of GPR68 in head and neck carcinogenesis (completed). Squamous cell carcinoma of ( the head and neck (SCCHN) is one of the deadliest cancers with more than 14,000 expected deaths, and greater than 65,000 new cases in the United States (US) in 2020. Former and active smokers as well as users of smokeless tobacco products are at the highest risk of developing this invasive cancer. Mortality from SCCHN could be reduced through the identification of new molecular targets associated with SCCHN carcinogenesis. GPR68, also known as ovarian cancer G protein-coupled receptor 1 (OGR1), is a pH-sensing G-protein-coupled receptor (GPCR) that responds to extracellular acidity, a defining hallmark of the tumor microenvironment (TME). GPR68 is expressed in several tissues such as esophagus, stomach, intestine, bone, endothelium, immune system, lungs and cancer. Emerging evidence has revealed that GPR68 may play crucial roles in tumorigenesis, tumor growth, and metastasis. This project explored a novel role for GPR68 in SCCHN carcinogenesis. Manuscript: https://www.nature.com/articles/s41598-023-27546-y
MyD88-dependent regulation of intestinal epithelial cells by dietary fat. Obesity is linked to metabolic syndrome and changes in intestinal bacteria. Intestinal epithelial cells (IECs) separate the luminal and internal compartments of the gastrointestinal (GI) tract, and are the first point of contact with gut bacteria. Disruptions in the epithelial barrier contribute to inflammatory disorders from microbial translocation. Although high fat diets (HFD) are known to increase GI permeability and alter the composition of intestinal microbes, the effects of HFD on IEC function are not fully characterized. Microbial products stimulate toll-like receptors (TLRs) on immune cells, initiating an inflammatory signaling cascade mediated by an adaptor named MyD88. This study is testing the hypothesis that dietary fat regulates IEC gene expression in a MyD88-dependent manner.
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