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
Hemozoin-inducible proinflammatory events in vivo: potential role in malaria infection.Journal Article
J Immunol, 172 (5), pp. 3101-10, 2004, ISSN: 0022-1767.
Blockade of S100A8 and S100A9 suppresses neutrophil migration in response to lipopolysaccharide.Journal Article
J Immunol, 171 (5), pp. 2602-9, 2003, ISSN: 0022-1767.
Role of S100A8 and S100A9 in neutrophil recruitment in response to monosodium urate monohydrate crystals in the air-pouch model of acute gouty arthritis.Journal Article
Arthritis Rheum, 48 (8), pp. 2310-20, 2003, ISSN: 0004-3591.
The calcium-binding protein S100A12 induces neutrophil adhesion, migration, and release from bone marrow in mouse at concentrations similar to those found in human inflammatory arthritis.Journal Article
Clin Immunol, 107 (1), pp. 46-54, 2003, ISSN: 1521-6616.
Proinflammatory activities of S100: proteins S100A8, S100A9, and S100A8/A9 induce neutrophil chemotaxis and adhesion.Journal Article
J Immunol, 170 (6), pp. 3233-42, 2003, ISSN: 0022-1767.
HIV-1 transcription and virus production are both accentuated by the proinflammatory myeloid-related proteins in human CD4+ T lymphocytes.Journal Article
J Immunol, 169 (6), pp. 3307-13, 2002, ISSN: 0022-1767.
The S100 family heterodimer, MRP-8/14, binds with high affinity to heparin and heparan sulfate glycosaminoglycans on endothelial cells.Journal Article
J Biol Chem, 277 (5), pp. 3658-65, 2002, ISSN: 0021-9258.
Activation of human neutrophils in vitro and dieldrin-induced neutrophilic inflammation in vivo.Journal Article
J Leukoc Biol, 70 (3), pp. 367-73, 2001, ISSN: 0741-5400.
The use of lymphocyte function-associated antigen (LFA)-1-deficient mice to determine the role of LFA-1, Mac-1, and alpha4 integrin in the inflammatory response of neutrophils.Journal Article
J Exp Med, 194 (2), pp. 219-26, 2001, ISSN: 0022-1007.
Activation of human neutrophils by technical toxaphene.Journal Article
Clin Immunol, 98 (1), pp. 46-53, 2001, ISSN: 1521-6616.
- Biology of S100A8 and S100A9 proteins in Human Acute Myeloid Leukemia, Subvention, Instituts de recherche en santé du Canada, Subvention Projet, from 2019-10-01 to 2024-09-30
- Centre de recherche du 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
Recently finished projects
- Centre de recherche en arthrite de l'Université Laval, Subvention, Institutionnel - BDR, BDR - Entités de recherche en émergence, from 2019-01-01 to 2020-01-31
- 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