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Comment
. 2014 Aug 13;16(2):145-147.
doi: 10.1016/j.chom.2014.07.014.

What lies within: coinfections and immunity

Blossom Damania  1 , Dirk P Dittmer  2
Affiliations
Comment

What lies within: coinfections and immunity

Blossom Damania et al. Cell Host Microbe. .

Abstract

Helminth-induced immunomodulation is thought to influence the outcome of secondary infections. Osborne et al. (2014) and Reese et al. (2014) demonstrate that helminth infection impacts viral infections by tilting the immune system toward Th2/M2 immune regulatory responses that dampen Th1/M1 antiviral responses as well as promote reactivation of latent herpesviruses.

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Figures

Figure 1
Figure 1
Helminth infection induces type 2 immune responses and the production of IL-4, which effectively induces the AAMacs pathway. Panel A summarizes the systemic release ofYM1 in proximal macrophages and their reprogramming into AAMacs. This has local as well as systemic consequences resulting in increased susceptibility to intestinal (norovirus) and respiratory (influenza virus) infection. Panel B shows reactivation of latent MHV-68 through a direct interaction between STAT6 and the promoter of the viral immediate early transactivator RTA (Orf50). IL-4/IL-13 counteracts IFN-γ, which normally restricts MHV-68 reactivation from macrophages.
Figure 1
Figure 1
Helminth infection induces type 2 immune responses and the production of IL-4, which effectively induces the AAMacs pathway. Panel A summarizes the systemic release ofYM1 in proximal macrophages and their reprogramming into AAMacs. This has local as well as systemic consequences resulting in increased susceptibility to intestinal (norovirus) and respiratory (influenza virus) infection. Panel B shows reactivation of latent MHV-68 through a direct interaction between STAT6 and the promoter of the viral immediate early transactivator RTA (Orf50). IL-4/IL-13 counteracts IFN-γ, which normally restricts MHV-68 reactivation from macrophages.
See this image and copyright information in PMC

Comment on

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