Aran S. D. Shaunak
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Aran S. D. Shaunak has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
David L. Williams
Department of Surgery, Center for Inflammation, Infectious Disease and Immunity, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, United States
1 shared publicationE. Suzanne Cohen
Biopharmaceutical Research Division, AstraZeneca, Cambridge, United Kingdom
1 shared publicationJ. S. Hill Gaston
Department of Medicine, School of Clinical Medicine, Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom
1 shared publication- Jane Caroline Goodall
Department of Medicine, University of Cambridge, Cambridge, UK
1 shared publication - Martin Steinmetz
Department of Internal Medicine, Division of Cardiology, Angiology and Internal Emergency Medicine, Department of Medicine, Knappschaft Kliniken University Hospital Bochum, Ruhr University Bochum, Bochum, Germany
1 shared publication Matthew J. Elder
Department of Medicine, School of Clinical Medicine, Addenbrookes Hospital, University of Cambridge, Cambridge, United Kingdom
1 shared publication
Latest Publications
- Open Access
- 8 May 2019
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 10, 921
Dendritic Cell-Derived TSLP Negatively Regulates HIF-1α and IL-1β During Dectin-1 Signaling
Thymic stromal lymphopoietin (TSLP) is a functionally pleotropic cytokine important in immune regulation, and TSLP dysregulation is associated with numerous diseases. TSLP is produced by many cell types, but has predominantly been characterized as a secreted factor from epithelial cells which activates dendritic cells (DC) that subsequently prime T helper (TH) 2 immunity. However, DC themselves make significant amounts of TSLP in response to microbial products, but the functional role of DC-derived TSLP remains unclear. We show that TSLPR signaling negatively regulates IL-1β production during dectin-1 stimulation of human DC. This regulatory mechanism functions by dampening Syk phosphorylation and is mediated via NADPH oxidase-derived ROS, HIF-1α and pro-IL-1β expression. Considering the profound effect TSLPR signaling has on the metabolic status and the secretome of dectin-1 stimulated DC, these data suggest that autocrine TSLPR signaling could have a fundamental role in modulating immunological effector responses at sites removed from epithelial cell production of TSLP.
- 8 May 2019
- Published by Frontiers Media SA in Frontiers in Immunology
- Vol. 10, 921
Open AccessDendritic Cell-Derived TSLP Negatively Regulates HIF-1α and IL-1β During Dectin-1 Signaling
Thymic stromal lymphopoietin (TSLP) is a functionally pleotropic cytokine important in immune regulation, and TSLP dysregulation is associated with numerous diseases. TSLP is produced by many cell types, but has predominantly been characterized as a secreted factor from epithelial cells which activates dendritic cells (DC) that subsequently prime T helper (TH) 2 immunity. However, DC themselves make significant amounts of TSLP in response to microbial products, but the functional role of DC-derived TSLP remains unclear. We show that TSLPR signaling negatively regulates IL-1β production during dectin-1 stimulation of human DC. This regulatory mechanism functions by dampening Syk phosphorylation and is mediated via NADPH oxidase-derived ROS, HIF-1α and pro-IL-1β expression. Considering the profound effect TSLPR signaling has on the metabolic status and the secretome of dectin-1 stimulated DC, these data suggest that autocrine TSLPR signaling could have a fundamental role in modulating immunological effector responses at sites removed from epithelial cell production of TSLP.