Full text loading...
Chapter 24 : Acquired Immunity to Intracellular Protozoa
Category: Immunology; Clinical Microbiology
Ebook: Choose a downloadable PDF or ePub file. Chapter is a downloadable PDF file. File must be downloaded within 48 hours of purchase
The control of pathogenic intracellular protozoa is dependent upon both an innate and acquired (or adaptive) immune response. Innate immune responses play an important role by controlling the early replication of parasites, giving time for acquired immunity to develop, although innate immune responses are rarely able to provide sufficient protection to prevent disease. Understanding how protective immunity can be induced, as well as knowing the mechanisms used by these intracellular parasites to avoid destruction, is critical for the development of new therapies as well as vaccines. This chapter investigates the acquired immune responses important in the control of four intracellular protozoans: Plasmodium, Leishmania, Toxoplasma gondii, and Trypanosoma cruzi. Acquired immunity to malaria is frequently described as being either antiparasite immunity, encompassing effector mechanisms that kill and clear parasites or parasite-infected cells, or clinical (or antitoxic) immunity. It is widely believed that acquired immunity to malaria rapidly wanes in the absence of frequent reinfection. A recent review suggests that previously immune individuals who become infected after spending long periods in nonendemic areas may develop mild-to-moderate symptoms of malaria despite having very low parasitemia.
Maintenance of immunity in the presence of persistent parasites. Several protozoal infections resolve their disease without eliminating all of the parasites, but nevertheless contain the parasites at low numbers and are resistant to reinfection. This resistance can be maintained by the continual generation of effector T cells from naïve T cells, a central memory pool of T cells, as well as from resting effector T cells.
Age/transmission-dependent acquisition of antimalarial immunity. Immunity to malaria is acquired gradually over time; in endemic areas, this means that immunity is acquired as a function of age (number of years exposed). Resistance to severe disease and death is acquired most rapidly. Immunity to mild clinical disease is acquired next and correlates with the induction of immune responses that limit parasite density. Immunity to infection, per se, as evidenced by less frequent episodes of asymptomatic, low density infection, is eventually acquired but in most individuals is only partial, meaning that episodes of infection can persist throughout life but rarely cause clinical signs or symptoms. Different immune mechanisms are believed to provide clinical and antiparasitic immunity (see text). Diagram adapted from original by B. M. Greenwood, London School of Hygiene and Tropical Medicine.
Antimalarial immune mechanisms. The immune effector mechanisms that are believed to confer immunity to different parasite life cycle stages are shown. This summary is based on the weight of evidence from very large numbers of experimental studies in animal models, in vitro studies with human cells, and immunoepidemiological studies. In no case is the actual mode of protection definitively known and there are currently no absolute immune correlates of protection against malaria infection or disease.