ABSTRACT
Resistance to infection essentially can be described as being of two types, innate and acquired, dependent upon activation of host immunity with secondary enhanced killing of amastigotes within infected cells. Macrophage function has also been shown to be diminished in stressed animals; the decreased MHC class II antigen expression on macrophages in these models in turn leads to impaired antigen-presenting-function, decreased lymphocyte activation, and thus decreased immunity to infection. Investigations of possible biochemical mechanisms behind the phenomenon of conditioning of immune responses, or stress-induced alteration of immunity, are rare. In a conditioning model in which mice were exposed to physical stressors, along with a number of environmental cues associated with that stressor, it was found subsequently that mere exposure to the cues at the same time as the animals received an immunological challenge would produce documented inhibition of the immune response when compared with non-stressed animals, or animals stressed but not re-exposed to the cues.
