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Grant: Doctoral Research Award: Canada Graduate Scholarships

Queen's University (Kingston, Ontario)

$105,000.00

The Role of IL-23 and the IL-23/Th17 Axis in the Pathophysiology of Endometriosis

FY 2022-23

Summary
Endometriosis (EM) is a common debilitating gynecological condition characterized by the presence/growth of tissue, resembling that which normally lines the uterus, in abnormal sites outside the uterine cavity. This disease has a broad range of symptoms, which are often not EM-specific. Furthermore, societal stigma and normalization of female pain surrounding menstrual/reproductive issues may make patients reluctant to discuss or disclose symptoms. Due to this, patient symptoms are often dismissed or misinterpreted by doctors, resulting in a long diagnostic period. To further complicate this, even once diagnosed there are no non-invasive, non-hormonal, or curative therapeutic options existing today. This highlights the great need to further research on EM. Though the exact cause of EM is unknown, there are a few theories as to the origin of this disease, such as Sampson's widely accepted theory of retrograde menstruation. This theory suggests that during menstruation, menstrual blood is refluxed backward through the fallopian tubes into the pelvic cavity where it can persist and form lesions. However, as this process occurs in most menstruating individuals, and yet not all those with retrograde menstruation have EM, other factors such as immune system dysfunction are thought to allow lesions to survive and grow. Specifically, it is thought that the immune system is not able to maintain a normal balance in EM, resulting in abnormal levels and/or functions of important cells and molecules of the immune system. Thus, my project focuses particularly on a subset of white blood cells (T-helper 17 cells) and how an immune system molecule (interleukin-23) may cause these cells to become harmful in EM, contributing to disease. Ultimately, using human patients and mouse models of EM, this research will allow us to gain a greater understanding of the dysfunctional immune environment in EM, and so, may aid in our development of adequate therapy options for patients with EM.
Program
Doctoral Research Award: Canada Graduate Scholarships
Location
Ontario, Canada
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
476104
Name
Sisnett Danielle J
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Doctoral Research Awards - A
Projecttitle
The Role of IL-23 and the IL-23/Th17 Axis in the Pathophysiology of Endometriosis
Programtype2
Studentship Programs
Orgnameinp2
Queen's University (Kingston, Ontario)
Cihramount2
$105,000
Cihrequipment2
$0
Programname2
Doctoral Research Award: Canada Graduate Scholarships
Keyworddelim
Cytokines; Endometriosis; Immune Dysfunction; Infertility; Th17 Cell Pathologies; Therapeutic Development
Abstract
Endometriosis (EM) is a common debilitating gynecological condition characterized by the presence/growth of tissue, resembling that which normally lines the uterus, in abnormal sites outside the uterine cavity. This disease has a broad range of symptoms, which are often not EM-specific. Furthermore, societal stigma and normalization of female pain surrounding menstrual/reproductive issues may make patients reluctant to discuss or disclose symptoms. Due to this, patient symptoms are often dismissed or misinterpreted by doctors, resulting in a long diagnostic period. To further complicate this, even once diagnosed there are no non-invasive, non-hormonal, or curative therapeutic options existing today. This highlights the great need to further research on EM. Though the exact cause of EM is unknown, there are a few theories as to the origin of this disease, such as Sampson's widely accepted theory of retrograde menstruation. This theory suggests that during menstruation, menstrual blood is refluxed backward through the fallopian tubes into the pelvic cavity where it can persist and form lesions. However, as this process occurs in most menstruating individuals, and yet not all those with retrograde menstruation have EM, other factors such as immune system dysfunction are thought to allow lesions to survive and grow. Specifically, it is thought that the immune system is not able to maintain a normal balance in EM, resulting in abnormal levels and/or functions of important cells and molecules of the immune system. Thus, my project focuses particularly on a subset of white blood cells (T-helper 17 cells) and how an immune system molecule (interleukin-23) may cause these cells to become harmful in EM, contributing to disease. Ultimately, using human patients and mouse models of EM, this research will allow us to gain a greater understanding of the dysfunctional immune environment in EM, and so, may aid in our development of adequate therapy options for patients with EM.
Competitiondate
202211
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Sisnett, Danielle J
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $105,000~ $0~
Queen's University (Kingston, Ontario) - $105,000 Gra… | Canada Spends