Immune response and immunopathology during toxoplasmosis

Abstract

Toxoplasma gondii is a protozoan parasite of medical and veterinary significance that is able to infect any warm-blooded vertebrate host. In addition to its importance to public health, several inherent features of the biology of T. gondii have made it an important model organism to study host-pathogen interactions. One factor is the genetic tractability of the parasite, which allows studies on the microbial factors that affect virulence and allows the development of tools that facilitate immune studies. Additionally, mice are natural hosts for T. gondii, and the availability of numerous reagents to study the murine immune system makes this an ideal experimental system to understand the functions of cytokines and effector mechanisms involved in immunity to intracellular microorganisms. In this article, we will review current knowledge of the innate and adaptive immune responses required for resistance to toxoplasmosis, the events that lead to the development of immunopathology, and the natural regulatory mechanisms that limit excessive inflammation during this infection.

Figure 1. Potential antigen presentation pathways

A. Antigen may be acquired through the phagocytosis of infected cells, intact parasites, parasite antigens, or through the endocytosis of parasite debris. B. Antigen may also be acquired by infected cells through the release of soluble antigens from the parasite, or through the sampling of antigens from the parasitophorous vacuole, which may be mediated by fusion of the parasitopherous vacuole with the endoplasmic reticulum. Antigens may also be injected into the host cell through abortive invasion events.