Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Research Project (R01)
Project #
5R01AR033887-11
Application #
2078944
Study Section
General Medicine A Subcommittee 2 (GMA)
Project Start
1984-12-01
Project End
1999-03-31
Budget Start
1996-04-01
Budget End
1997-03-31
Support Year
11
Fiscal Year
1996
Total Cost
Indirect Cost
Name
University of North Carolina Chapel Hill
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
078861598
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Kuan, Anita P; Cohen, Philip L (2005) p53 is required for spontaneous autoantibody production in B6/lpr lupus mice. Eur J Immunol 35:1653-60
Cohen, Philip L; Caricchio, Roberto (2004) Genetic models for the clearance of apoptotic cells. Rheum Dis Clin North Am 30:473-86, viii
Suh, Chang-Hee; Freed, John H; Cohen, Philip L (2003) T cell reactivity to MHC class II-bound self peptides in systemic lupus erythematosus-prone MRL/lpr mice. J Immunol 170:2229-35
Caricchio, Roberto; McPhie, Lenese; Cohen, Philip L (2003) Ultraviolet B radiation-induced cell death: critical role of ultraviolet dose in inflammation and lupus autoantigen redistribution. J Immunol 171:5778-86
Freed, J H; Marrs, A; VanderWall, J et al. (2000) MHC class II-bound self peptides from autoimmune MRL/lpr mice reveal potential T cell epitopes for autoantibody production in murine systemic lupus erythematosus. J Immunol 164:4697-705
Weintraub, J P; Cohen, P L (1999) Ectopic expression of B7-1 (CD80) on T lymphocytes in autoimmune lpr and gld mice. Clin Immunol 91:302-9
Caricchio, R; Kovalenko, D; Kaufmann, W K et al. (1999) Apoptosis provoked by the oxidative stress inducer menadione (Vitamin K(3)) is mediated by the Fas/Fas ligand system. Clin Immunol 93:65-74
Caricchio, R; Cohen, P L (1999) Spontaneous and induced apoptosis in systemic lupus erythematosus: multiple assays fail to reveal consistent abnormalities. Cell Immunol 198:54-60
Fecho, K; Cohen, P L (1998) Fas ligand (gld)- and Fas (lpr)-deficient mice do not show alterations in the extravasation or apoptosis of inflammatory neutrophils. J Leukoc Biol 64:373-83
Booker, J K; Reap, E A; Cohen, P L (1998) Expression and function of Fas on cells damaged by gamma-irradiation in B6 and B6/lpr mice. J Immunol 161:4536-41

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