Clinically and experimentally, cell-mediated immune responses are impaired in individuals who consume excessive amounts of alcohol for prolonged periods of time, resulting in a predilection for infection by intracellular pathogens. Alcohol's effect occurs during the cognitive phase of the immune response when the antigen presenting cell (APC) and T helper (Th) cell interact. Downstream events are affected, such that IL-12 production by APC and subsequent IFN-gamma production by Th are diminished. What is the extent of alcohol's effect on APC subpopulations (macrophages, dendritic cells, and B cells) and their ability to stimulate naive and memory Th responses? In vivo, the alcohol-mediated immune deficit may be reversed by immunizing ethanol- consuming mice with antigen-pulsed APCs from non-ethanol consuming mice.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Individual Predoctoral NRSA for M.D./Ph.D. Fellowships (ADAMHA) (F30)
Project #
5F30AA005527-02
Application #
2893983
Study Section
Special Emphasis Panel (ZAA1-DD (01))
Program Officer
Isaki, Leslie
Project Start
1999-09-11
Project End
Budget Start
1999-09-11
Budget End
2000-09-10
Support Year
2
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Northwestern University at Chicago
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
005436803
City
Chicago
State
IL
Country
United States
Zip Code
60611