Fachbereich Veterinärmedizin



    IL10-Deficiency in CD4⁺ T Cells Exacerbates the IFNγ and IL17 Response During Bacteria Induced Colitis (2015)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Seiffart, Virginia
    Zoeller, Julia
    Klopfleisch, Robert (WE 12)
    Wadwa, Munisch
    Hansen, Wiebke
    Buer, Jan
    Riedel, Christian
    Westendorf, Astrid M
    Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology; 36(4) — S. 1259–1273
    ISSN: 1015-8987
    URL (Volltext): http://edocs.fu-berlin.de/docs/receive/FUDOCS_document_000000023029
    DOI: 10.1159/000430295
    Pubmed: 26160212
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
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    Abstract / Zusammenfassung

    IL10 is a key inhibitor of effector T cell activation and a mediator of intestinal homeostasis. In addition, IL10 has emerged as a key immunoregulator during infection with various pathogens, ameliorating the excessive T-cell responses that are responsible for much of the immunopathology associated with the infection. Because IL10 plays an important role in both intestinal homeostasis and infection, we studied the function of IL10 in infection-associated intestinal inflammation.

    Wildtype mice and mice deficient in CD4+ T cell-derived or regulatory T cells-derived IL10 were infected with the enteric pathogen Citrobacter (C.) rodentium and analyzed for the specific immune response and pathogloy in the colon.

    We found that IL10 expression is upregulated in colonic tissue after infection with C. rodentium, especially in CD4+ T cells, macrophages and dendritic cells. Whereas the deletion of IL10 in regulatory T cells had no effect on C. rodentium induced colitis, infection of mice deficient in CD4+ T cell-derived IL10 exhibited faster clearance of the bacterial burden but worse colitis, crypt hyperplasia, and pathology than did WT mice. In addition, the depletion of CD4+ T cell-derived IL10 in infected animals was accompanied by an accelerated IFNγ and IL17 response in the colon.

    Thus, we conclude that CD4+ T cell-derived IL10 is strongly involved in the control of C. rodentium-induced colitis. Interference with this network could have implications for the treatment of infection-associated intestinal inflammation.