Grant: Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships
University of British Columbia
$105,000.00
RELM-B: the missing link between gut microbes and T cell activation during T cell transfer induced colitis?
FY 2014-15
Summary
Inflammatory Bowel Diseases (IBD), comprising Ulcerative Colitis and Crohn's Disease, are lifelong illnesses characterized by severe intestinal inflammation and ulceration leading to abdominal pain, weight loss, diarrhea and rectal bleeding. Canada has the highest IBD rates in the world, with 30% of patients diagnosed before the age of 20. Although medical research has made significant advances in treating IBD, many of the current therapies available have variable response rates as well as potential allergic reactions associated with their use. The lack of therapies available likely reflects our limited understanding of the mechanisms by which IBD develops.
A strong theory for why IBD may develop, however, is that a group of white blood cells, known as CD4+ T cells, develop a reaction to commensal bacteria in our intestines resulting in inflammation and consequent tissue damage. How these cells get to the intestine and why they react to gut bacteria remains unknown. Our lab has found that a certain immune molecule known as RELM-B, released by mucus-producing cells in the intestine, is significantly increased during a mouse model of intestinal inflammation caused by injecting in these CD4+ T cells (making it a highly relevant model of IBD). Interestingly, we've also found that mice lacking RELM-B are protected from developing inflammation after CD4+ T cell injection. The goal of my research is to use this IBD model to understand the effects of this molecule RELM-B on changes to the gut bacteria during inflammation, as well as its role in activating the reactive CD4+ T cells causing the tissue damage. Ultimately my studies will improve our understanding of how IBD develops and potentially identify a novel and specific target for therapeutic intervention in IBD, benefitting both children and adults worldwide.
Department
Program
Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships
Recipient
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
327868
Name
Bhinder Ganive
Region
British Columbia
Country
Canada
Orgtype
Research Institution; Institution Paid
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Doctoral Research Awards - A
Projecttitle
RELM-B: the missing link between gut microbes and T cell activation during T cell transfer induced colitis?
Programtype2
Studentship Programs
Orgnameinp2
University of British Columbia
Cihramount2
$105,000
Cihrequipment2
$0
Programname2
Doctoral Award - Frederick Banting and Charles Best Canada Graduate Scholarships
Keyworddelim
Commensal Bacteria; Goblet Cells; Inflammation; Inflammatory Bowel Disease; Innate Immunity; Reistin-Like Molecules; T Cell Transfer-Induced Colitis; T Cells; Ulcerative Colitis
Abstract
Inflammatory Bowel Diseases (IBD), comprising Ulcerative Colitis and Crohn's Disease, are lifelong illnesses characterized by severe intestinal inflammation and ulceration leading to abdominal pain, weight loss, diarrhea and rectal bleeding. Canada has the highest IBD rates in the world, with 30% of patients diagnosed before the age of 20. Although medical research has made significant advances in treating IBD, many of the current therapies available have variable response rates as well as potential allergic reactions associated with their use. The lack of therapies available likely reflects our limited understanding of the mechanisms by which IBD develops.
A strong theory for why IBD may develop, however, is that a group of white blood cells, known as CD4+ T cells, develop a reaction to commensal bacteria in our intestines resulting in inflammation and consequent tissue damage. How these cells get to the intestine and why they react to gut bacteria remains unknown. Our lab has found that a certain immune molecule known as RELM-B, released by mucus-producing cells in the intestine, is significantly increased during a mouse model of intestinal inflammation caused by injecting in these CD4+ T cells (making it a highly relevant model of IBD). Interestingly, we've also found that mice lacking RELM-B are protected from developing inflammation after CD4+ T cell injection. The goal of my research is to use this IBD model to understand the effects of this molecule RELM-B on changes to the gut bacteria during inflammation, as well as its role in activating the reactive CD4+ T cells causing the tissue damage. Ultimately my studies will improve our understanding of how IBD develops and potentially identify a novel and specific target for therapeutic intervention in IBD, benefitting both children and adults worldwide.
Competitiondate
201410
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Bhinder, Ganive
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $105,000~ $0~