Publications by authors named "J Tocker"
Metabolites produced in the human gut are known modulators of host immunity. However, large-scale identification of metabolite-host receptor interactions remains a daunting challenge. Here, we employed computational approaches to identify 983 potential metabolite-target interactions using the Inflammatory Bowel Disease (IBD) cohort dataset of the Human Microbiome Project 2 (HMP2).
View Article and Find Full Text PDFThe cytokine TNFSF14 [homologous to Lymphotoxin, exhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEM, a receptor expressed on T lymphocytes (LIGHT)] has been shown in mouse models to be important for development of lung tissue remodeling that is characteristic of asthma, idiopathic pulmonary fibrosis (IPF), and systemic sclerosis (SSc). However, its cellular targets are not fully delineated. In the present report, we show that LTβR and HVEM, the receptors for LIGHT, are constitutively expressed in primary human lung fibroblasts (HLFs).
View Article and Find Full Text PDFArticle Synopsis
- Food allergies (FA) are growing in prevalence and currently lack approved treatments, with pro-T2 cytokines (IL-25, IL-33, TSLP) playing a key role in their development.
- Researchers tested whether blocking these pro-T2 cytokines with monoclonal antibodies (mAbs) could prevent the induction and maintenance of FA in mice, finding that while FA development could be inhibited, established FA could not be suppressed by a single mAb alone.
- A combination of mAbs targeting all three cytokines was necessary for optimal suppression of FA, suggesting that targeting pro-T2 cytokines may be a potential treatment strategy for human food allergies.
Lung epithelial cells are considered important sources of inflammatory molecules and extracellular matrix proteins that contribute to diseases such as asthma. Understanding the factors that stimulate epithelial cells may lead to new insights into controlling lung inflammation. This study sought to investigate the responsiveness of human lung epithelial cells to the TNF family molecules LIGHT and lymphotoxin αβ (LTαβ).
View Article and Find Full Text PDFIL-17RA Signaling in Airway Inflammation and Bronchial Hyperreactivity in Allergic Asthma.
Am J Respir Cell Mol Biol
December 2015
Article Synopsis
- * In experiments using mouse models, blocking IL-17RA, IL-17RB, or IL-25 led to reduced airway inflammation and hyperreactivity, suggesting these pathways are important in asthma progression.
- * IL-17A and IL-25 both increase the contractility of bronchial smooth muscle, with IL-17A showing stronger effects in asthma patients, indicating that targeting the IL-17 pathway might offer new treatment options for asthma.