Immunity to Parasitic Worms

Helminth infection provides a unique challenge to the host immune system. Not only are helminths complex multicellular organisms, but they have intricate life cycles with multiple developmental stages, several of which may coexist in the infected host. In most cases, the host response to helminth infection is characterized by eosinophilia, increased serum immunoglobulin (Ig) E and IgG4, and mast cell hyperplasia. However, the role of these responses in immunity to infection is complex and depends on a variety of factors including the site of the parasite in the host (intestinal versus tissue invasive), the particular helminth species, and the stage of the life cycle examined. Immune responses may prevent infection entirely in an uninfected host (protective immunity), limit further infection in an already infected host (concomitant immunity) or, when directed at specific life cycle stages, interrupt transmission. It is the balance of these factors and characteristics of the host, such as genetic background, prenatal exposure to parasite antigens, and the duration and intensity of exposure, that determine the outcome of exposure (i.e. immunity, infection, pathology). As a rule, helminths do not multiply in the host, but produce offspring that must exit the host to continue the parasite life cycle. Consequently, helminth species have developed complex and redundant mechanisms to produce chronic infection despite abundant evidence of immune recognition by the host. These include sequestration in anatomical locations relatively impervious to immune attack, molecular mimicry, shedding of antigenic surface proteins, and downregulation of the host immune response to helminth antigens, producing a state of parasite-specific immune tolerance. In this article, characteristic features of the host’s protective immune response to helminth infection will be discussed as well as some of the strategies used by different helminth species to evade these responses. Finally, the relationship between the protective host immune response to helminths and the pathological consequences of infection will be explored. Protective Immunity