M
Mireille S. Potentier
Researcher at University of Calgary
Publications - 4
Citations - 586
Mireille S. Potentier is an academic researcher from University of Calgary. The author has contributed to research in topics: Inflammasome & Innate immune system. The author has an hindex of 2, co-authored 4 publications receiving 513 citations.
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Journal ArticleDOI
NLRP3 inflammasome plays a key role in the regulation of intestinal homeostasis
Simon A. Hirota,Jeffrey Ng,Alan Lueng,Maitham A. Khajah,Ken Kuljit S. Parhar,Yan Li,Victor Lam,Mireille S. Potentier,Kelvin Ng,Misha Bawa,Donna-Marie McCafferty,Kevin P. Rioux,Subrata Ghosh,Ramnik J. Xavier,Sean P. Colgan,Jürg Tschopp,Daniel A. Muruve,Justin A. MacDonald,Paul L. Beck +18 more
TL;DR: An essential role for the NLRP3 inflammasome is confirmed in the maintenance of intestinal homeostasis through its regulation of innate protective processes and biological insight into disease mechanisms associated with increased risk of CD in individuals withNLRP3 mutations is provided.
Journal ArticleDOI
Clostridium difficile Toxin–Induced Inflammation and Intestinal Injury Are Mediated by the Inflammasome
Jeffrey Ng,Simon A. Hirota,Olaf Gross,Yan Li,Annegret Ulke–Lemee,Mireille S. Potentier,L. Patrick Schenck,Akosua Vilaysane,Mark E. Seamone,Hanping Feng,Glen D. Armstrong,Jürg Tschopp,Justin A. MacDonald,Daniel A. Muruve,Paul L. Beck +14 more
TL;DR: TcdA and TcdB trigger IL-1beta release by activating an ASC-containing inflammasome, a response that contributes to toxin-induced inflammation and damage in vivo.
Journal ArticleDOI
Exaggerated IL-15 and Altered Expression of foxp3+ Cell-Derived Cytokines Contribute to Enhanced Colitis in Nlrp3−/− Mice
Simon A. Hirota,Aito Ueno,Sarah E. Tulk,Helen M. Becker,L. Patrick Schenck,Mireille S. Potentier,Yan Li,Subrata Ghosh,Daniel A. Muruve,Justin A. MacDonald,Paul L. Beck +10 more
TL;DR: In this article, the loss of NLRP3 might be altering the function of regulatory T cells, a major source of IL-10, and was associated with increased expression of colonic IL-15 and increased surface expression on LP dendritic cells.