Philippe Tessier studied at Laval University, the John Curtin School of Medical Research (Australian National University) and the University of Adelaide, followed by a post-doctoral fellowship at the Imperial Cancer Research Fund (United Kingdom). He has been a researcher at the Centre de recherche du CHU de Québec – Laval University since 1999, and a professor at the Department of Microbiology-Infectiology and Immunology of the Laval University School of Medicine.
Professor Tessier studies the biological activities of the proteins S100A8 and S100A9, two small proteins expressed by neutrophils, monocytes, and activated endothelial and epithelial cells. These proteins are secreted during inflammation and activate the immune response. His research indicates that S100A8 and S100A9 have opposite functions: S100A8 is anti-inflammatory and inhibits myeloid cell differentiation, while S100A9 is pro-inflammatory and induces the differentiation of precursors of neutrophils and monocytes. He studies the roles of these proteins in autoimmune diseases such as rheumatoid arthritis, psoriasis, and Crohn’s disease, in immune responses to solid tumors, and in the differentiation of leukemia cells.
Auto-inflammatory diseases are monogenic orphan diseases (<10,000 cases per syndrome worldwide) usually caused by defects in the genes regulating innate immunity. These diseases are characterized by recurrent, unprovoked inflammation (fever, abdominal pain, rash, arthralgia). High plasma concentrations of S100A8 and S100A9 are often found in patients with auto-inflammatory diseases. In collaboration with Professor Martin Pelletier and Dr. Anne-Laure Chetaille, Prof. Tessier is currently studying the roles of S100A8 and S100A9 in these diseases, to develop a diagnostic test to facilitate the treatment of these patients.
2705, boulevard Laurier
Canada G1V 4G2
Data not available
Quinoline-3-carboxamides such as tasquinimod are not specific inhibitors of S100A9.Journal Article
Blood Adv, 2 (10), pp. 1170-1171, 2018, ISSN: 2473-9529.
S100A8/A9 and sRAGE kinetic after polytrauma; an explorative observational study.Journal Article
Scand J Trauma Resusc Emerg Med, 25 (1), pp. 114, 2017.
S100A9 potentiates the activation of neutrophils by the etiological agent of gout, monosodium urate crystals.Journal Article
J Leukoc Biol, 102 (3), pp. 805-813, 2017, ISSN: 0741-5400.
S100A9 induces differentiation of acute myeloid leukemia cells through TLR4.Journal Article
Blood, 129 (14), pp. 1980-1990, 2017, ISSN: 0006-4971.
IL-23 induced in keratinocytes by endogenous TLR4 ligands polarizes dendritic cells to drive IL-22 responses to skin immunization.Journal Article
J Exp Med, 213 (10), pp. 2147-66, 2016, ISSN: 0022-1007.
- Centre hospitalier universitaire de Québec - CHU de Québec-Université Laval, Subvention, Centre hospitalier universitaire de Québec - Université Laval, Centres de recherche affiliés, from 2017-01-01 to 2099-12-31
- Immunosuppressive function of S100A8 in arthritis., Subvention, Instituts de recherche en santé du Canada, Subvention de fonctionnement, from 2014-07-01 to 2019-06-30
- The characterization of MICL, a novel negative regulator of the immune response in arthritis., Subvention, Instituts de recherche en santé du Canada, Subvention de fonctionnement, from 2015-07-01 to 2020-06-30
Recently finished projects
- Analyse du profil de cytokines par les cellules sanguines de patients atteints de maladies auto-inflammatoires orphelines, Subvention, Le Grand Défi Pierre Lavoie, Subvention pour projet de recherche sur une maladie héréditaire orpheline, from 2016-10-01 to 2017-09-30
- Centre de recherche en infectiologie, Subvention, Institutionnel - BDR, BDR - Centres de recherche reconnus, from 1996-06-01 to 2018-04-30
- Development of an assay to better diagnose and treat auto-inflammatory patients., Subvention, Rare Disease Foundation, Microgrant program, from 2015-05-25 to 2016-05-01
- Traitement de la leucémie myéloïde aiguë par la protéine S100A9., Subvention, Fondation de l'Université Laval, from 2015-10-01 to 2017-09-30