Host protective roles of type 2 immunity: parasite killing and tissue repair, flip sides of the same coin.

Judith Allen, Tara Sutherland

Research output: Contribution to journalArticlepeer-review

187 Citations (Scopus)

Abstract

Metazoan parasites typically induce a type 2 immune response, characterized by T helper 2 (Th2) cells that produce the cytokines IL-4, IL-5 and IL-13 among others. The type 2 response is host protective, reducing the number of parasites either through direct killing in the tissues, or expulsion from the intestine. Type 2 immunity also protects the host against damage mediated by these large extracellular parasites as they migrate through the body. At the center of both the innate and adaptive type 2 immune response, is the IL-4Rα that mediates many of the key effector functions. Here we highlight the striking overlap between the molecules, cells and pathways that mediate both parasite control and tissue repair. We have proposed that adaptive Th2 immunity evolved out of our innate repair pathways to mediate both accelerated repair and parasite control in the face of continual assault from multicellular pathogens. Type 2 cytokines are involved in many aspects of mammalian physiology independent of helminth infection. Therefore understanding the evolutionary relationship between helminth killing and tissue repair should provide new insight into immune mechanisms of tissue protection in the face of physical injury.
Original languageEnglish
Pages (from-to)329-340
JournalSeminars in Immunology
Volume26
Issue number4
DOIs
Publication statusPublished - 1 Aug 2014

Bibliographical note

095831, Wellcome Trust, United Kingdom
MR/J001929/1, Medical Research Council, United Kingdom
MR/K01207X/1, Medical Research Council, United Kingdom,

Acknowledgments
JEA and TES are funded by Medical Research Council UK grants, MR/J001929/1 and MR/K01207X/1 and supported by the Wellcome Trust funded Centre for Immunity, Infection and Evolution.

Keywords

  • Eosinophils
  • Helminths
  • IL-4Rα
  • Macrophages
  • Th2 cells
  • Wound repair

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