Immune optimization refers to the tailoring of immune effector functions to optimize the clearance of particular pathogens.
The immune system of organisms help them survive infections by pathogenic microbes. Just as evolutionary pressures lead to the selection of pathogens that are capable of evading immune responses, evolution should select for the ability of organisms to alter their immune responses to favor effector mechanisms that are appropriate for the clearance of the detected pathogen.
In other words, if you sense a bacteria, your immune response would be geared towards killing bacteria. If you sense you've been infected with fungi, you'd respond with anti-fungal functions, etc.
Something like this is known to function. Locksley, et al. demonstrated that Leishmania is able to elicit one of two polar T-helper responses, depending on the strain of mouse that was infected. This Th1/Th2 polarity has a dramatic impact on the ability of the mouse to survive infection. Similarly, the kinds of immune cells that appear at sites of infection depend on the kind of microbe that is causing the infection.
Because adaptive immune receptors generate specificity de novo during maturation, they cannot link ligand specificity to evolutionarily selected spectrum of immune responses. Therefore, immune optimization must be mediated through innate immune receptors who's ligand specificity is genetically encode.
I'm not sure I'll keep calling this phenomenon immune optimization. It can also be called immune instruction, as in the innate immune system instructing the acquired immune system what to do.
A part of fhayashi's Node your PhD. dissertation program.