Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
1R01AI040181-01
Application #
2077087
Study Section
Experimental Immunology Study Section (EI)
Project Start
1996-08-01
Project End
1997-07-31
Budget Start
1996-08-01
Budget End
1997-07-31
Support Year
1
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
Boston Medical Center
Department
Type
DUNS #
005492160
City
Boston
State
MA
Country
United States
Zip Code
02118

  Publications

Kaku, Hiroaki; Cheng, Kai Fan; Al-Abed, Yousef et al. (2014) A novel mechanism of B cell-mediated immune suppression through CD73 expression and adenosine production. J Immunol 193:5904-13
Kaku, Hiroaki; Rothstein, Thomas L (2009) Fas apoptosis inhibitory molecule enhances CD40 signaling in B cells and augments the plasma cell compartment. J Immunol 183:1667-74
Kaku, Hiroaki; Rothstein, Thomas L (2009) Fas apoptosis inhibitory molecule expression in B cells is regulated through IRF4 in a feed-forward mechanism. J Immunol 183:5575-81
Barrington, Robert A; Schneider, Thomas J; Pitcher, Lisa A et al. (2009) Uncoupling CD21 and CD19 of the B-cell coreceptor. Proc Natl Acad Sci U S A 106:14490-5
Guo, Benchang; Tumang, Joseph R; Rothstein, Thomas L (2009) B cell receptor crosstalk: B cells express osteopontin through the combined action of the alternate and classical BCR signaling pathways. Mol Immunol 46:587-91
Mineva, Nora D; Rothstein, Thomas L; Meyers, John A et al. (2007) CD40 ligand-mediated activation of the de novo RelB NF-kappaB synthesis pathway in transformed B cells promotes rescue from apoptosis. J Biol Chem 282:17475-85