This program project has assembled molecular biologist, immunologist, population geneticist andclinical scientist to investigate the mechanism of co-stimulatory responses in patients with MS and type 1diabetes, and examine the hypothesis that a genetic predisposition for alterations in co-stimulatory signalleads to heightened inflammatory responses that in part underlies the pathophysiology of autoimmunediseases. To accomplish these goals, an administrative core is requested to ensure that financial activitiesamong project participants are in compliance with the appropriate NIH policies and guidelines throughout theproject period and to facilitate the report of our findings on an annual basis to the NIH. Additionally, animportant function of the administrative core will be the arrangement of monthly conference calls among thePPG participants and arranging the bi-annual meetings of the advisory board. Thus funding theadministrative core is important to accomplish the goals of the PPG.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI039671-13
Application #
7609522
Study Section
Special Emphasis Panel (ZAI1-GB-I (M2))
Project Start
2008-02-01
Project End
2010-01-31
Budget Start
2008-02-01
Budget End
2009-01-31
Support Year
13
Fiscal Year
2008
Total Cost
$92,815
Indirect Cost
Name
Brigham and Women's Hospital
Department
Type
DUNS #
030811269
City
Boston
State
MA
Country
United States
Zip Code
02115
Ponath, Gerald; Lincoln, Matthew R; Levine-Ritterman, Maya et al. (2018) Enhanced astrocyte responses are driven by a genetic risk allele associated with multiple sclerosis. Nat Commun 9:5337
Sumida, Tomokazu; Lincoln, Matthew R; Ukeje, Chinonso M et al. (2018) Activated ?-catenin in Foxp3+ regulatory T cells links inflammatory environments to autoimmunity. Nat Immunol 19:1391-1402
Meyer Zu Horste, Gerd; Przybylski, Dariusz; Schramm, Markus A et al. (2018) Fas Promotes T Helper 17 Cell Differentiation and Inhibits T Helper 1 Cell Development by Binding and Sequestering Transcription Factor STAT1. Immunity 48:556-569.e7
Chihara, Norio; Madi, Asaf; Kondo, Takaaki et al. (2018) Induction and transcriptional regulation of the co-inhibitory gene module in T cells. Nature 558:454-459
Ordovas-Montanes, Jose; Dwyer, Daniel F; Nyquist, Sarah K et al. (2018) Allergic inflammatory memory in human respiratory epithelial progenitor cells. Nature 560:649-654
Mead, Benjamin E; Ordovas-Montanes, Jose; Braun, Alexandra P et al. (2018) Harnessing single-cell genomics to improve the physiological fidelity of organoid-derived cell types. BMC Biol 16:62
Wu, Chuan; Chen, Zuojia; Xiao, Sheng et al. (2018) SGK1 Governs the Reciprocal Development of Th17 and Regulatory T Cells. Cell Rep 22:653-665
Lucca, Liliana E; Hafler, David A (2017) Resisting fatal attraction: a glioma oncometabolite prevents CD8+ T cell recruitment. J Clin Invest 127:1218-1220
Joller, Nicole; Kuchroo, Vijay K (2017) Tim-3, Lag-3, and TIGIT. Curr Top Microbiol Immunol 410:127-156
Nylander, Alyssa N; Ponath, Gerald D; Axisa, Pierre-Paul et al. (2017) Podoplanin is a negative regulator of Th17 inflammation. JCI Insight 2:

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