Optimality Analysis of Th1/Th2 Immune Responses During Microparasite–Macroparasite Co-infection, with Epidemiological Feedbacks

School of Biological Sciences, University of Liverpool, Biosciences Building, Crown Street, Liverpool, L69 7ZB, UK.
Parasitology (Impact Factor: 2.56). 07/2008; 135(7):841-53. DOI: 10.1017/S0031182008000310
Source: PubMed


Individuals are typically co-infected by a diverse community of microparasites (e.g. viruses or protozoa) and macroparasites (e.g. helminths). Vertebrates respond to these parasites differently, typically mounting T helper type 1 (Th1) responses against microparasites and Th2 responses against macroparasites. These two responses may be antagonistic such that hosts face a 'decision' of how to allocate potentially limiting resources. Such decisions at the individual host level will influence parasite abundance at the population level which, in turn, will feed back upon the individual level. We take a first step towards a complete theoretical framework by placing an analysis of optimal immune responses under microparasite-macroparasite co-infection within an epidemiological framework. We show that the optimal immune allocation is quantitatively sensitive to the shape of the trade-off curve and qualitatively sensitive to life-history traits of the host, microparasite and macroparasite. This model represents an important first step in placing optimality models of the immune response to co-infection into an epidemiological framework. Ultimately, however, a more complete framework is needed to bring together the optimal strategy at the individual level and the population-level consequences of those responses, before we can truly understand the evolution of host immune responses under parasite co-infection.

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Available from: Andrew Fenton, Jan 23, 2015
    • "Bergmann-Leitner et al. 2009). Nematode-induced suppression of Th1 immunity can reduce production of such antibodies and prolong malaria infection (Fenton et al. 2008). Here, we report the first analysis that disentangles effects of resource limitation and immune facilitation upon parasite dynamics during co-infection, thereby achieving a rare identification of determinants of ecological dynamics across replicate ecosystems. "
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    • "The second subgroup of studies modeled population plasticity of Th1/Th2 cell responses. These models included the processes of cross-regulation of Th1/Th2 cell responses either directly by cell-to-cell interactions or via production of Th1/Th2 cytokines (Fishman and Perelson, 1999; Yates et al., 2000, 2004; Bergmann et al., 2001, 2002; Fenton et al., 2008; Eftimie et al., 2010; Groß et al., 2011). Some of these models offered a theoretical explanation of the switch from an initially dominant pathogens-specific Th2 response to a later dominant Th1 response (or vice versa). "
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