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Th2 and eosinophil responses suppress inflammatory arthritis

Author

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  • Zhu Chen

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg
    Anhui Medical University Affiliated Provincial Hospital)

  • Darja Andreev

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg)

  • Katharina Oeser

    (University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU))

  • Branislav Krljanac

    (University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU))

  • Axel Hueber

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg)

  • Arnd Kleyer

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg)

  • David Voehringer

    (University Hospital Erlangen and Friedrich-Alexander University Erlangen-Nuremberg (FAU))

  • Georg Schett

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg)

  • Aline Bozec

    (University Hospital Erlangen and Friedrich Alexander University of Erlangen-Nuremberg)

Abstract

Th2–eosinophil immune responses are well known for mediating host defence against helminths. Herein we describe a function of Th2–eosinophil responses in counteracting the development of arthritis. In two independent models of arthritis, Nippostrongylus brasiliensis infection leads to Th2 and eosinophil accumulation in the joints associated with robust inhibition of arthritis and protection from bone loss. Mechanistically, this protective effect is dependent on IL-4/IL-13-induced STAT6 pathway. Furthermore, we show that eosinophils play a central role in the modulation of arthritis probably through the increase of anti-inflammatory macrophages into arthritic joints. The presence of these pathways in human disease is confirmed by detection of GATA3-positive cells and eosinophils in the joints of rheumatoid arthritis patients. Taken together, these results demonstrate that eosinophils and helminth-induced activation of the Th2 pathway axis effectively mitigate the course of inflammatory arthritis.

Suggested Citation

  • Zhu Chen & Darja Andreev & Katharina Oeser & Branislav Krljanac & Axel Hueber & Arnd Kleyer & David Voehringer & Georg Schett & Aline Bozec, 2016. "Th2 and eosinophil responses suppress inflammatory arthritis," Nature Communications, Nature, vol. 7(1), pages 1-12, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11596
    DOI: 10.1038/ncomms11596
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    Cited by:

    1. Darja Andreev & Katerina Kachler & Mengdan Liu & Zhu Chen & Brenda Krishnacoumar & Mark Ringer & Silke Frey & Gerhard Krönke & David Voehringer & Georg Schett & Aline Bozec, 2024. "Eosinophils preserve bone homeostasis by inhibiting excessive osteoclast formation and activity via eosinophil peroxidase," Nature Communications, Nature, vol. 15(1), pages 1-20, December.

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