Brugia malayi is a human filarial infection, which can grow in mice. The PI hypothesizes that resistance of Brugia malayi is composed of an initial B dependent, T independent protective immune response which constrains initial parasite growth and that a subsequent T dependent, IL-4 mediated defense results in subsequent more effective immunity. The PI will use a combination of mice, genetically deficient in specific aspects of their immune response, and the adoptive transfer of specific cell populations into deficient mice, to investigate the mechanisms of the postulated immunoprotective events. The PI suggests that if B cells are important in this model, they may also be important in human disease and the specific modulation of their responses by B dependent immunogens may form a basis of an immunoprophylactic vaccine for humans.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
5R01AI039075-07
Application #
6624636
Study Section
Special Emphasis Panel (ZRG1-BM-1 (01))
Program Officer
Wali, Tonu M
Project Start
1996-07-01
Project End
2005-11-30
Budget Start
2002-12-01
Budget End
2003-11-30
Support Year
7
Fiscal Year
2003
Total Cost
$405,509
Indirect Cost
Name
University of Connecticut
Department
Pathology
Type
Schools of Medicine
DUNS #
022254226
City
Farmington
State
CT
Country
United States
Zip Code
06030