The Regulatory Role of the Antigen-Presenting Cell in the Development of Hepatic Immunopathology during Infection with Schistosoma mansoni

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Abstract
A recent meeting held in Berlin (2nd Teupitz Colloquium) focused on the striking ability of mononuclear phagocytes to either stimulate or inhibit a variety of immune and immunopathological responses, and ascribed a distinctive phenotype to the antigen-presenting cells (APC) when exercising these opposite functions. Thus, the phenotype and secretory profile of APC associated with ‘classical activation’ is achieved following stimulation with pro-inflammatory cytokines such as interferon-γ, and leads to full T cell activation. On the other hand, it has long been known that T cells may also be downregulated after interacting with certain APC. Many of such APC, originally simply thought to lack or have lost their stimulatory potential, are now thought to be in a state of ‘alternative activation’, which is associated with a different phenotype and secretory profile that can typically be induced with anti-inflammatory reagents, including the cytokines IL-4, IL-10 and IL-13. The purpose of this article is to analyze the immunopathological events that characterize the infection with Schistosoma mansoni in context with these distinct APC activation pathways. Available evidence from human and experimental data suggests that a desirable outcome of the APC during this parasitic disease is to attain ‘alternative activation’, which serves to promote and sustain a Th-2-polarized immune response associated with a more favorable anti-inflammatory and host-protective environment.

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