Dr. Fawzi Aoudjit is a senior scientist at the CHU de Québec Research Centre and a professor at the department of microbiology-infectiology and immunology of the Laval University School of Medicine. His research program seeks to understand the mechanisms controlling T cell activity in tissues during inflammatory/autoimmune diseases and cancer, with a focus on the role of the adhesion molecules that bind to extracellular matrix, the integrins. T cells play an important role in the adaptive immune response, but are also critical to the development of inflammatory diseases, and could become malignant and lead to cancer. Recent work by Dr. Aoudjit’s group significantly contributed to understand the importance of extracellular matrix-binding integrins in the regulation of T cell activation and the development of immune response. Along these lines, Dr. Aoudjit and his team have shown that the collagen-binding integrin alpha2beta1 is an important pathway in Th17 cell activation and in the development of arthritis. These studies were highlighted in the news bulletin ‘Immune regulation news’. Dr. Aoudjit received several acknowledgements for his work among which, the New Investigator Award from the Canadian Institutes of Health Research, in 2004.
The current objectives aim to
- understand how collagen receptors such as integrins and discoïdin domain receptors interact to promote the survival and migration of T cell subsets in inflammatory tissues; two critical T cell functions necessary to the development of inflammation, as well as to mounting an anti-cancer immune response.
- determine the role of integrins in the development of lymphoblastic leukemia by investigating their implication in the tissue dissemination of leukemic T cells, and in their resistance to chemotherapy; two cancer features that limit the efficacy of anti-cancer treatments.
The implication of these receptors in the development of inflammatory diseases and cancer is being investigated in human T cell models, in preclinical models of autoimmune diseases, leukemia, and in models of anti-cancer immunity, as well as at the clinical level with the collaboration of clinicians.
In addition to advancing knowledge, these studies aim at the discovery of novel therapeutic targets and treatments for autoimmune diseases and cancer.
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The Purinergic Receptor P2X4 Promotes Th17 Activation and the Development of ArthritisJournal Article
J Immunol, 208 (5), 2022.
VLA-4 Induces Chemoresistance of T Cell Acute Lymphoblastic Leukemia Cells via PYK2-Mediated Drug EffluxJournal Article
Cancers (Basel), 13 (14), 2021.
Deletion of and Enhances Skin Hyperplasia and Promotes the Th17 Response in Imiquimod-Induced PsoriasisJournal Article
J Immunol, 206 (3), 2021.
Assessment of Arf6 Deletion in PLB-985 Differentiated in Neutrophil-Like Cells and in Mouse Neutrophils: Impact on Adhesion and MigrationJournal Article
Mediators Inflamm, 2020 , 2020.
CD154 inhibits death of T cells via a Cis interaction with the α5β1 integrinJournal Article
PLoS One, 15 (8), 2020.
Exacerbated intestinal inflammation in P2Y deficient mice is associated with Th17 activationJournal Article
Biochim Biophys Acta Mol Basis Dis, 1865 (10), 2019.
Cell adhesion to collagen promotes leukemia resistance to doxorubicin by reducing DNA damage through the inhibition of Rac1 activationJournal Article
Sci Rep, 9 (1), 2019.
Beta1 integrin blockade overcomes doxorubicin resistance in human T-cell acute lymphoblastic leukemiaJournal Article
Cell Death Dis, 10 (5), 2019.
Enhanced myelopoiesis and aggravated arthritis in S100a8-deficient miceJournal Article
PLoS One, 14 (8), 2019.
Alpha2beta1 Integrin (VLA-2) Protects Activated Human Effector T Cells From Methotrexate-Induced ApoptosisJournal Article
Front Immunol, 9 , 2018.
- Expression and function of discoidin domain receptor 1 in T cells, from 2017-04-01 to 2023-03-31
- Role of discoidin domain receptor 1 in T cell migration and arthritis, from 2020-01-01 to 2022-12-31
Recently finished projects
- Profil moléculaire sanguin de patientes souffrant de lupus, from 2019-04-01 to 2021-03-31