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Grant: Doctoral Research Award: Canada Graduate Scholarships

University of British Columbia

$120,000.00

Hic1 in the maintenance of lung CD4+ T cells (TRM) in allergic asthma

FY 2024-25

Summary
Asthma is a long-lasting lung disease that impacts 300 million individuals worldwide. The condition is characterized by lung inflammation, overproduction of mucus, and narrowed airways, primarily caused by a specific group of immune cells known as T helper (Th) cells. Recent research highlights the critical role of a subset of these Th cells, named tissue-resident memory T cells (TRM), found in the lungs of individuals with asthma. These TRM cells are pivotal in recurring asthma episodes as they quickly react to allergens, distinguishing them from other memory T cells circulating in the body. Developing therapies focusing on TRM cells presents a promising avenue for asthma treatment, aiming to diminish the swift allergenic responses initiated by these cells. A key player in this process may be a molecule named Hic1, prevalent in TRM cells and responsible for regulating gene activity within cells. Hic1 helps inactivate various cells and influences the residence of TRM cells in many tissues. We think that Hic1 is vital in supporting the TRM cells in the lungs, and the absence of Hic1 may lead to the reduction of TRM cells, potentially abolishing the responses to allergens. This research could set a foundation for potential treatments for asthma and other diseases in which TRM cells play a crucial role. In summary, delving deeper into the functions of TRM cells and the Hic1 molecule could pave the way for innovative asthma and TRM-dependent disease treatments, fostering hope for enhanced disease management.
Program
Doctoral Research Award: Canada Graduate Scholarships
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
519138
Name
Kim Taehyun
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Doctoral Research Awards - A
Projecttitle
Hic1 in the maintenance of lung CD4+ T cells (TRM) in allergic asthma
Programtype2
Studentship Programs
Orgnameinp2
University of British Columbia
Cihramount2
$120,000
Cihrequipment2
$0
Programname2
Doctoral Research Award: Canada Graduate Scholarships
Keyworddelim
Asthma; Immunology; Tissue Resident Memory T Cells
Abstract
Asthma is a long-lasting lung disease that impacts 300 million individuals worldwide. The condition is characterized by lung inflammation, overproduction of mucus, and narrowed airways, primarily caused by a specific group of immune cells known as T helper (Th) cells. Recent research highlights the critical role of a subset of these Th cells, named tissue-resident memory T cells (TRM), found in the lungs of individuals with asthma. These TRM cells are pivotal in recurring asthma episodes as they quickly react to allergens, distinguishing them from other memory T cells circulating in the body. Developing therapies focusing on TRM cells presents a promising avenue for asthma treatment, aiming to diminish the swift allergenic responses initiated by these cells. A key player in this process may be a molecule named Hic1, prevalent in TRM cells and responsible for regulating gene activity within cells. Hic1 helps inactivate various cells and influences the residence of TRM cells in many tissues. We think that Hic1 is vital in supporting the TRM cells in the lungs, and the absence of Hic1 may lead to the reduction of TRM cells, potentially abolishing the responses to allergens. This research could set a foundation for potential treatments for asthma and other diseases in which TRM cells play a crucial role. In summary, delving deeper into the functions of TRM cells and the Hic1 molecule could pave the way for innovative asthma and TRM-dependent disease treatments, fostering hope for enhanced disease management.
Competitiondate
202411
Approvedterm2
3 yrs 0 mth
Pinamesdelim
Kim, Taehyun
Approvedterm
3 ans 0 mois
Cihrcontribution2
~ $120,000~ $0~