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Grant: Master's Award: Canada Graduate Scholarships

York University (Toronto, Ontario)

$17,500.00

Investigating the role of tumor necrosis factor receptor associated factor 1 in animal models of inflammatory arthritis and lipopolysaccharide-induced septic shock

FY 2022-23

Summary
Inflammation is an important immune system process as white blood cells protects us from foreign invaders and facilitate healing. However, chronic and uncontrolled inflammation can lead to serious health conditions such as cardiovascular disease, cancer, and autoimmune diseases like rheumatoid arthritis (RA). RA is a chronic autoimmune disease that develops due to abnormal inflammatory responses, eventually contributing to the destruction of cartilage and bone. This disease affects approximately 1.2% of Canadians aged 16 years and older, with a higher incidence and prevalence in females compared to males. It’s important to diagnose and treat RA as early as possible to slow the progression of the disease. To date, there is no cure for RA and the treatments offered only alleviate the symptoms. Recent studies in our lab show that the tumor necrosis factor receptor associated factor 1 (TRAF1) has a dichotomous role in the immune system, making it an excellent candidate to selectively target in the development of RA therapies. Interestingly, our lab has identified a mutation in TRAF1 in human monocyte cells that limits the activation of lymphocytes while reducing the production of pro-inflammatory cytokines in macrophages. My research project will be the first to use a genetically modified mice with this mutation to investigate the dichotomous role of TRAF1 in inflammatory diseases like RA. In this study, I will use a well-studied endotoxin to trigger an inflammatory response. I will then measure protection from excessive inflammation by employing techniques that determine the expression levels of key proteins involved in the inflammatory response. Cumulatively, my findings will create the foundation for designing novel methods to lower inflammation and improve RA prognosis.
Program
Master's Award: Canada Graduate Scholarships
Location
Ontario, Canada
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
490910
Name
Madahar Sahib S
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Prcname2
Special Cases - Awards Programs
Projecttitle
Investigating the role of tumor necrosis factor receptor associated factor 1 in animal models of inflammatory arthritis and lipopolysaccharide-induced septic shock
Programtype2
Studentship Programs
Orgnameinp2
York University (Toronto, Ontario)
Cihramount2
$17,500
Cihrequipment2
$0
Programname2
Master's Award: Canada Graduate Scholarships
Keyworddelim
Collagen-Induced Arthritis (Cia); Crispr/Cas9; Inflammation; Lipopolysaccharide (Lps); Lymphocytes; Macrophages; Nuclear Factor-Kappa B (Nf-Kb); Rheumatoid Arthritis; Sepsis; Traf1
Abstract
Inflammation is an important immune system process as white blood cells protects us from foreign invaders and facilitate healing. However, chronic and uncontrolled inflammation can lead to serious health conditions such as cardiovascular disease, cancer, and autoimmune diseases like rheumatoid arthritis (RA). RA is a chronic autoimmune disease that develops due to abnormal inflammatory responses, eventually contributing to the destruction of cartilage and bone. This disease affects approximately 1.2% of Canadians aged 16 years and older, with a higher incidence and prevalence in females compared to males. It’s important to diagnose and treat RA as early as possible to slow the progression of the disease. To date, there is no cure for RA and the treatments offered only alleviate the symptoms. Recent studies in our lab show that the tumor necrosis factor receptor associated factor 1 (TRAF1) has a dichotomous role in the immune system, making it an excellent candidate to selectively target in the development of RA therapies. Interestingly, our lab has identified a mutation in TRAF1 in human monocyte cells that limits the activation of lymphocytes while reducing the production of pro-inflammatory cytokines in macrophages. My research project will be the first to use a genetically modified mice with this mutation to investigate the dichotomous role of TRAF1 in inflammatory diseases like RA. In this study, I will use a well-studied endotoxin to trigger an inflammatory response. I will then measure protection from excessive inflammation by employing techniques that determine the expression levels of key proteins involved in the inflammatory response. Cumulatively, my findings will create the foundation for designing novel methods to lower inflammation and improve RA prognosis.
Competitiondate
202212
Approvedterm2
1 yr 0 mth
Pinamesdelim
Madahar, Sahib S
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $17,500~ $0~