Helminths: Immunoregulation and Inflammatory Diseases-Which Side Are Trichinella spp. and Toxocara spp. on?

Abstract

Macropathogens, such as multicellular helminths, are considered masters of immunoregulation due to their ability to escape host defense and establish chronic infections. Molecular crosstalk between the host and the parasite starts immediately after their encounter, which influences the course and development of both the innate and adaptive arms of the immune response. Helminths can modulate dendritic cells (DCs) function and induce immunosuppression which is mediated by a regulatory network that includes regulatory T (Treg) cells, regulatory B (Breg) cells, and alternatively activated macrophages (AAMs). In this way, helminths suppress and control both parasite-specific and unrelated immunopathology in the host such as Th1-mediated autoimmune and Th2-mediated allergic diseases. However, certain helminths favour the development or exacerbation of allergic responses. In this paper, the cell types that play an essential role in helminth-induced immunoregulation, the consequences for inflammatory diseases, and the contrasting effects of Toxocara and Trichinella infection on allergic manifestations are discussed.

Figure 1

Mechanisms involved in immunosuppression induced by helminths and its effect on allergic responses. Helminths can modulate dendritic cells (DCs) function and induce regulatory T (Treg) cells. Other cells from the regulatory network include regulatory B (Breg) cells and alternatively activated macrophages (AAMs). These cells create an immunosuppressive (⊣) environment in which increased expression of arginase 1 (Arg 1) in AAMs and the production of the cytokines IL-10 and TGF-β play an essential role in reducing allergic effector mechanisms.