Abstract
Parasitic infections are prevalent in both tropical and subtropical
areas. Most of the affected and/or exposed populations are living in
developing countries where control measures are lacking or inadequately applied.
Although significant progress has been made in our understanding of
the immune response to parasites, no definitive step has yet been successfully
done in terms of operational vaccines against parasitic diseases.
Evidence accumulated during the past few years suggests that the
pathology observed during parasitic infections is in part due to deregulation
of normal components of the immune system, mainly cytokines,
antibodies, and immune effector cell populations. A large number
of studies that illustrate how parasites can modify the host immune
system for their own benefit have been reported in both metazoan and
protozoan parasites. The first line of defense against foreign organisms
is barrier tissue such as skin, humoral factors, for instance the complement system
and pentraxin, which upon activation of the complement cascade
facilitate pathogen recognition by cells of innate immunity
such as macrophages and DC. However, all the major groups of parasites studied have been shown to contain and/or to release factors, which interfere with both arms of the host immune system. Even some astonishing observations relate to the production by some parasites of orthologues of mammalian cytokines. Furthermore, chronic parasitic infections have led to the immunosuppressive environment that correlates with increased levels of myeloid and T suppressor cells that may limit the success of immunotherapeutic strategies based on vaccination. This minireview briefly analyzes some of the current data related to the regulatory cells and molecules derived from parasites that affect cellular function and contribute to the polarization of the immune response of the host. Special attention is given to some of the data from our laboratory illustrating the role of immunomodulatory factors released by protozoan parasites, in the induction and perpetuation of chronic disease.