Atopic asthma and other allergic diseases are caused by a pathologic response of individuals to environmental antigens. To cure these diseases will require an understanding of the mechanisms that are required to initiate these immune responses and the mechanisms required to propagate them. One of the major paradigms that recent research in this field has generated is that both the initiation and propagation of allergic immune responses requires the interaction of different inflammatory cells. In addition, this interaction requires the exchange of information between these cells. Central to the exchange of information between cells involved in an allergic immune response is the use of signaling pathways to transmit these signals to the nucleus of the cells. This realization has begun to drive therapeutic research in the direction of altering these signaling pathways in order to modify the resultant allergic immune response. This Research Center seeks to understand the role of signaling pathways in allergic and asthmatic immune responses. In Project 1, Dr. Schindler proposes to study the role of STAT signaling in the development and function of Dendritic Cells (DC). In Project 2, Dr. Pernis will study the regulation of CD23 in normal and allergic humans. In Project 3, Dr. Clynes will study the role of Fc receptors in the initiation and propagation of allergic and asthmatic immune responses. In Project 4, Dr. Rothman will study how Pim kinases alter IL-4 signaling and how this alters allergic immune responses. In Project 5, Dr. Miller will study the immune response of the unborn child. The knowledge gained by this Center will improve our understanding of the signaling pathways required for an allergic immune response. A Scientific Core and an Administrative Core will support these projects. The Scientific Core will provide technical expertise and assistance in murine models of asthma and allergic immune responses. The Administrative Core will assist in organizing the Center?s activities.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI050514-05
Application #
6895290
Study Section
Special Emphasis Panel (ZAI1-NBS-I (M3))
Program Officer
Plaut, Marshall
Project Start
2001-08-27
Project End
2006-05-31
Budget Start
2005-06-01
Budget End
2006-05-31
Support Year
5
Fiscal Year
2005
Total Cost
$1,549,178
Indirect Cost
Name
Columbia University (N.Y.)
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
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Tsitoura, Daphne C; Rothman, Paul B (2004) Enhancement of MEK/ERK signaling promotes glucocorticoid resistance in CD4+ T cells. J Clin Invest 113:619-27

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