T-cell-specific deletion of gp130 renders the highly susceptible IL-10-deficient mouse resistant to intestinal nematode infection

Research output: Contribution to journalArticle

  • Authors:
  • Nicolas Fasnacht
  • Marina C. Greweling
  • Mariela Bollati-Fogolín
  • Angela Schippers
  • Werner Müller

Abstract

Gp130 is the common receptor of the IL-6 family of cytokines and is involved in many biological processes, including acute phase response, inflammation and immune reactions. To investigate the role of gp130 under inflammatory conditions, T-cell-specific conditional gp130 mice were first bred to the IL-10-deficient background and were then infected with the gastrointestinal nematode Trichuris muris. While IL-10-/- mice were highly susceptible to T. muris, developed amixed Th1/Th17 response and displayed severe inflammation of the caecum, infection of mice with an additional T-cell-specific deletion of gp130 signalling completely reversed the phenotype. These mice showed an accelerated worm expulsion that was associated with the rapid generation of a strong Th2 immune response and a significant increase in Foxp3-expressing Treg. Therefore, gp130 signalling in T cells regulates a switch between proinflammatory and pathogenic Th1/Th17 cells and regulatory Th2/Treg in vivo. Taken together, the data demonstrate that gp130 signalling in T cells is a positive regulator of inflammatory processes, favouring the Th1/Th17 axis. © 2009 Wiley-VCH Verlag GmbH & Co. KGaA.

Bibliographical metadata

Original languageEnglish
Pages (from-to)2173-2183
Number of pages10
JournalEuropean journal of immunology
Volume39
Issue number8
DOIs
Publication statusPublished - Aug 2009

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