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Review
. 2011 Feb;138(2):139-59.
doi: 10.1017/S0031182010001216. Epub 2010 Oct 15.

Acquired immune heterogeneity and its sources in human helminth infection

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Free PMC article
Review

Acquired immune heterogeneity and its sources in human helminth infection

C D Bourke et al. Parasitology. 2011 Feb.
Free PMC article

Abstract

Similarities in the immunobiology of different parasitic worm infections indicate that co-evolution of humans and helminths has shaped a common anti-helminth immune response. However, recent in vitro and immuno-epidemiological studies highlight fundamental differences and plasticity within host-helminth interactions. The 'trade-off' between immunity and immunopathology inherent in host immune responses occurs on a background of genetic polymorphism, variable exposure patterns and infection history. For the parasite, variation in life-cycle and antigen expression can influence the effector responses directed against them. This is particularly apparent when comparing gastrointestinal and tissue-dwelling helminths. Furthermore, insights into the impact of anti-helminthic treatment and co-infection on acquired immunity suggest that immune heterogeneity arises not from hosts and parasites in isolation, but also from the environment in which immune responses develop. Large-scale differences observed in the epidemiology of human helminthiases are a product of complex host-parasite-environment interactions which, given potential for exposure to parasite antigens in utero, can arise even before a parasite interacts with its human host. This review summarizes key differences identified in human acquired immune responses to nematode and trematode infections of public health importance and explores the factors contributing to these variations.

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Figures

Fig. 1
Fig. 1
Summary of the major CD4+ T cell differentiation pathways following activation in the periphery. Cytokines and transcription factors involved in T cell polarization are shown in boxes and within cells respectively. Effector cell types and cytokines associated with each CD4+ T cell phenotype are given adjacent to relevant cells. Th0 – naïve T cell, * RORγt – murine transcription factor, the human orthologue is RORC2. Figure adapted from Deenick and Tangyne (2007) and Diaz and Allen (2007).
Fig. 2
Fig. 2
The relationship between age and infection intensity in natural human helminthiases. (A) Mean W. bancrofti microfilaria (mf) count by age group (n=156, study area: Papua New Guinea, method: microscopy of 2 ml Giemsa-stained blood). Reprinted from the American Journal of Tropical Medicine and Hygiene (Day et al. 1991b), with permission from the managing editor. (B) Mean hookworm (A. duodenale and N. americanus) egg counts per gram faeces (EPG) by age group (n=631, study area: China, method: Kato-Katz thick smear). Reprinted from the Journal of Parasitology (Gandhi et al. 2001), with permission from Allen Press Publishing Services. (C) Mean T. trichiuris eggs per gram of faeces by age group (n=96, study area: Cameroon, method: Kato-Katz thick smear). Reprinted from the Journal of Infectious Diseases (Faulkner et al. 2002), with permission from the University of Chicago Press. (D) Age-infection intensity profiles of S. haematobium egg counts per 10 ml of urine from an area of low infection prevalence (dashed line) and an area of high infection prevalence (solid line) group (n=133 and 147, study area: Zimbabwe, method: filtration of 10 ml of urine) (re-drawn from Mutapi et al. 1997). Reprinted from Parasitology Today (Woolhouse, 1998), with permission from Elsevier and John Wiley and Sons Ltd.

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