B lymphocytes form an integral part of the immune system primarily through its ability to recognize and react against an infinite set of foreign antigens. Activation of B cells by antigen triggers an active immune response resulting in the production of antibodies that neutralize the invading antigen. In addition, as an effort to mount a full scale immune response, the activated B cells also secrete soluble factors to further recruit and activate other components of the immune system. While the ability of B cells to respond to antigen is crucial for maintaining health, its ability to dampen its activated state would soon after clearance of the invading antigen is of equal importance. Aberrant activation of B cells would result in an uncontrolled state of immunity, as evidenced in autoimmune diseases. The proposed study herein is to examine the molecular wiring that controls the activation of B cells. We will focus on dissection the regulatory potential of a central protein, Syk, which is implicated in triggering the activation signals for B cells. The result from these studies would provide a better understanding of the feedback control of B cell activation.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
1P01AI047330-01
Application #
6400345
Study Section
Special Emphasis Panel (ZAI1-NN-I (J2))
Project Start
2000-09-30
Project End
2004-08-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2000
Total Cost
$241,412
Indirect Cost
Name
Washington University
Department
Type
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Bui, Jack D; Carayannopoulos, Leonidas N; Lanier, Lewis L et al. (2006) IFN-dependent down-regulation of the NKG2D ligand H60 on tumors. J Immunol 176:905-13