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.
Research Projects
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
RC-709
Québec, Québec
Canada G1V 4G2
Latest news
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Cooperation between IL-7 Receptor and Integrin α2β1 (CD49b) Drives Th17-Mediated Bone Loss.
Journal ArticleJ Immunol, 195 (9), pp. 4198-209, 2015, ISSN: 0022-1767.
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Regulation of TLR3 Activation by S100A9.
Journal ArticleJ Immunol, 195 (9), pp. 4426-37, 2015, ISSN: 0022-1767.
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Secretion of S100A8, S100A9, and S100A12 by Neutrophils Involves Reactive Oxygen Species and Potassium Efflux.
Journal ArticleJ Immunol Res, 2015 , pp. 296149, 2015, ISSN: 2314-7156.
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Human S100A9 potentiates IL-8 production in response to GM-CSF or fMLP via activation of a different set of transcription factors in neutrophils.
Journal ArticleFEBS Lett, 588 (13), pp. 2141-6, 2014, ISSN: 0014-5793.
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Intracellular expression of inflammatory proteins S100A8 and S100A9 leads to epithelial-mesenchymal transition and attenuated aggressivity of breast cancer cells.
Journal ArticleAnticancer Agents Med Chem, 14 (1), pp. 35-45, 2014, ISSN: 1871-5206.
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DAMP molecule S100A9 acts as a molecular pattern to enhance inflammation during influenza A virus infection: role of DDX21-TRIF-TLR4-MyD88 pathway.
Journal ArticlePLoS Pathog, 10 (1), pp. e1003848, 2014, ISSN: 1553-7366.
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α2β1 integrin regulates Th17 cell activity and its neutralization decreases the severity of collagen-induced arthritis.
Journal ArticleJ Immunol, 191 (12), pp. 5941-50, 2013, ISSN: 0022-1767.
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S100A8/A9 proteins mediate neutrophilic inflammation and lung pathology during tuberculosis.
Journal ArticleAm J Respir Crit Care Med, 188 (9), pp. 1137-46, 2013, ISSN: 1073-449X.
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Modulation of monosodium urate crystal-induced responses in neutrophils by the myeloid inhibitory C-type lectin-like receptor: potential therapeutic implications.
Journal ArticleArthritis Res Ther, 15 (4), pp. R73, 2013, ISSN: 1478-6354.
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S100A8 and S100A9 induce cytokine expression and regulate the NLRP3 inflammasome via ROS-dependent activation of NF-κB(1.).
Journal ArticlePLoS ONE, 8 (8), pp. e72138, 2013.
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Active projects
- 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