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Th2 response polarization during infection with the helminth parasite Schistosoma mansoni

Authors

  • Edward J. Pearce,

    Corresponding author
    1. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
      ¶ Edward J Pearce
      203D Johnson Pavilion
      3610 Hamilton Walk
      Philadelphia, PA 19106-6076
      USA
      Tel.: +1 215 573 3493
      Fax: +1 215 8989 557
      E-mail: ejpearce@mail.med.upenn.edu
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  • Colleen M. Kane,

    1. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
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  • Jie Sun,

    1. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
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  • Justin J. Taylor,

    1. Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
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  • Amy S. McKee,

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      Present address: Department of Immunology, National Jewish Medical and Research Center, Denver, CO, USA.
  • Laura Cervi

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      Present address: Parasitology, Department of Clinical Biochemistry, Faculty of Chemical Sciences, National University of Cordoba, Cordoba, Argentina.

¶ Edward J Pearce
203D Johnson Pavilion
3610 Hamilton Walk
Philadelphia, PA 19106-6076
USA
Tel.: +1 215 573 3493
Fax: +1 215 8989 557
E-mail: ejpearce@mail.med.upenn.edu

Abstract

Summary:  T-helper 2 (Th2) cell responses play a critical role in protection against helminth infections. In the case of Schistosoma mansoni, an important helminth parasite of man, data from a mouse model of human disease have shown that Th2 responses are essential to allow host survival. In this infection, parasite eggs are the primary stimulus for Th2 response development. Recent work has shown that egg molecules exert multiple levels of control over the development of host interferon-γ-associated inflammatory responses. Soluble egg antigen inhibits the ability of dendritic cells to make interleukin-12 and induces Th2-polarized adaptive immune responses that in combination with regulatory T-cell responses effectively limit Th1 response development. In this article, we discuss the factors influencing Th2 response polarization during infection with S. mansoni.

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