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.
