Area:
Molecular Biology, Immunology, Human Development
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Booki Min is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2019 — 2021 |
Min, Booki |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Foxp3+ Regulatory T Cell-Dependent Treatment of Allergic Inflammation by Glucocorticoids @ Northwestern University At Chicago
Abstract Asthma is a chronic inflammatory disease of the airways, affecting >25 million Americans. The annual economic cost for asthma exceeds 50 billion dollars, making asthma one of the most common and costly disease. Allergen specific Th2 type CD4 T cell activation and eosinophil infiltration are hallmarks of asthmatic inflammation. Oral or inhaled glucocorticoids have been the frontline treatment to effectively manage asthma for more than 50 years. Yet, the precise mechanisms underlying glucocorticoid-mediated treatment are not well understood. In addition, a cohort of asthmatic patients develops steroid-resistant asthma. Unlike conventional eosinophil-dominant Th2 type inflammation, steroid-resistant asthmatic inflammation is associated with neutrophilic infiltration with effector CD4 T cells displaying Th17 type signature. The current application is built upon unexpected observations that synthetic glucocorticoid, dexamethasone, fails to inhibit eosinophilic airway inflammation in the absence of Foxp3+ Tregs, a CD4 T cell subset that plays a central role in regulating immunity and tolerance. Adoptive Treg transfer into this condition restores dexamethasone treatment effects, supporting the role of Tregs. We also found that neutrophilic airway inflammation model that is dexamethasone resistant is attenuated upon treating with dexamethasone combined with IL-27, a cytokine essential for Treg suppressive functions. Dexamethasone/IL-27-mediated treatment of neutrophilic inflammation also failed in Treg-depleted or in Treg-specific Il27ra-/- mice, suggesting key roles of Tregs and of IL-27 signaling in Tregs. These preliminary results have led us to propose that Dex signaling induces Treg suppressive functions that limit eosinophilic inflammatory responses whereas control of neutrophilic inflammatory responses by Dex requires additional signals conferred by IL-27 to the Tregs. Three specific aims are proposed to test the hypothesis. Aim 1 is to test the hypothesis that that Dex downregulates eosinophilic airway inflammation by targeting Tregs. Aim 2 is to test the hypothesis that neutrophilic inflammation subverts Dex-induced Treg control of airway inflammation, resulting in Dex resistance. Aim 3 is to test the hypothesis that IL-27 signaling improves Dex responsiveness in Tregs to inhibit Dex-resistant neutrophilic inflammation. Completing the proposed studies will uncover the previously unknown mechanisms by which Tregs regulate both GC susceptible and GC resistant allergic airway inflammation, opening new opportunities to develop novel approaches to improve GC?s therapeutic efficacy and to overcome GC resistance by targeting Tregs.
|
0.939 |