CD8+ T cells play a critical role in controlling viral as well as intracellular bacterial and parasitic infections. In recent years considerable evidence has accumulated demonstrating the key role CD8+ T cells play in controlling tumor growth. The multiple functions of the CD8 component of cellular immunity are executed by three different classes of CD8 + T cells: naive, effector, and memory cells. Little, however is known about the changes' of gene expression that occur in antigen specific lymphocytes during viral infection. Acute infection is accompanied by massive expansion of naive cells to become effector cells. After antigen clearance 95- 98% of the effector cells will die. The surviving cells are memory cells and will confer protective immunity for the life of the mouse. We will determine changes in gene expression by performing quantitative Reverse Transcription-Polymerase Chain Reaction (qRT- PCR) on antigen specific lymphocytes isolated using recombinant MHC class I tetramers. This reagent will allow us to isolate antigen specific cells from a physiologically relevant situation without in vitro manipulation. Analysis of gene expression will allow us to develop rational strategies to dissect molecular mechanisms of CD8 function which is critical for vaccinations and immunotherapies.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32AI010249-01A1
Application #
6012901
Study Section
Special Emphasis Panel (ZRG1-EVR (01))
Program Officer
Prograis, Lawrence J
Project Start
1999-08-01
Project End
Budget Start
1999-08-01
Budget End
2000-07-31
Support Year
1
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Emory University
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
042250712
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Grayson, J M; Murali-Krishna, K; Altman, J D et al. (2001) Gene expression in antigen-specific CD8+ T cells during viral infection. J Immunol 166:795-9