The role of the innate immune system in pulmonary fibrosis, remains imperfectly understood. In other systems it is established that components of the innate immune system shape the more precise response of the adaptive immune system. Using a well described animal model of subacute pulmonary inflammation and fibrosis, the role of two of the Toll-Like Receptors, major components of the innate immune sytem and the specific influence each has on T lymphocyte differentiation, will be examined. Specifically, Aim 1 will describe the role of TLR2 in turning T cells away from a protective Th1 pathway of development, and Specific Aim 2 will demonstrate the role of TLR4 in producing T regulatory cells that protect from lung injury. Pulmonary fibrosis is the end stage of a wide range of diverse diseases, and leads to progressive respiratory failure and death. Currently understanding of why this occurs, and how to stop this process, is very limited, and better understanding will allow more useful therapies.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32HL094034-02
Application #
7668361
Study Section
Special Emphasis Panel (ZRG1-F10-H (21))
Program Officer
Colombini-Hatch, Sandra
Project Start
2008-08-01
Project End
2010-07-31
Budget Start
2009-08-01
Budget End
2010-07-31
Support Year
2
Fiscal Year
2009
Total Cost
$59,402
Indirect Cost
Name
Johns Hopkins University
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21218