Adaptive immunity and genetics of the host immune response

Immunity to T. gondii is complex, with aspects of innate and adaptive immune responses playing important effector roles. The innate immune system is also important in driving and dictating the quality of the adaptive immune response. The ability of T. gondii to infect any cell means that disease can be systemic and affect many organs, but in some cases certain organs, including the brain, eye, or intestine, have the predominant pathology. These individual organs are studied in detail using animal, most often murine, models of disease. The strong influence of host genetics on this disease process is evident from early studies, and is exploited to identify immunological functional correlates of protection and pathology. The influence of T. gondii genetics on the pathogenesis of both murine and human T. gondii infection has become increasingly evident in recent years. In experimental studies, the route and lifecycle stage used to initiate infection is varied according to convenience or scientific rationale, or to induce particular disease manifestations, and must also be noted when considering studies in the literature. It is also important to try to correlate findings of animal models with clinical findings and studies of human materials.