Regulation of the host immune system by helminth parasites

Abstract

Helminth parasite infections are associated with a battery of immunomodulatory mechanisms that affect all facets of the host immune response to ensure their persistence within the host. This broad-spectrum modulation of host immunity has intended and unintended consequences, both advantageous and disadvantageous. Thus the host can benefit from suppression of collateral damage during parasite infection and from reduced allergic, autoimmune, and inflammatory reactions. However, helminth infection can also be detrimental in reducing vaccine responses, increasing susceptibility to coinfection and potentially reducing tumor immunosurveillance. In this review we will summarize the panoply of immunomodulatory mechanisms used by helminths, their potential utility in human disease, and prospective areas of future research.

Keywords: Allergy; infection; pathology; therapy; tolerance.

Fig 1

Immune system–parasite interactions during helminth infections. A, Blockade of innate sensing and alarmin production, such as inhibiting Toll-like receptor (TLR) responses of dendritic cells, thereby impairing inflammatory T_H1/T_H17 development, and abrogating epithelial cell production of IL-33, thereby pre-empting the type 2 response. ILC2, Type 2 innate lymphoid cell. B, Modulation of the adaptive immune response, promoting Treg cell differentiation either directly through production of TGF-β–like mimics (TGM) or indirectly by inducing host TGF-β and retinoic acid (RA) from DCs and macrophages. C, Modification of bystander immune responses in the infected host.