Monocytes/macrophages and/or neutrophils are the target of IL-10 in the LPS endotoxemia model

Marina C. Pils, Fabio Pisano, Nicolas Fasnacht, Jan Michael Heinrich, Lothar Groebe, Angela Schippers, Björn Rozell, Robert S. Jack, Werner Müller

    Research output: Contribution to journalArticlepeer-review

    Abstract

    IL-10 is a potent regulator of the innate and adaptive immune responses. Several cell types produce IL-10 and its receptor chains and these may regulate different immune responses. Here we report that inactivation of the IL-10 receptor (IL-10R1) gene in mice leads to an increased susceptibility to chemically induced colitis as in the classical IL-10-deficient mutant. To identify the cells regulated by IL-10 in immune responses, we generated several cell type specific IL-10R1-deficient mutants. We show that, in an IL-10-dependent LPS model of endotoxemia, dampening of the immune response requires expression of IL-10R1 in monocytes/macrophages and/or neutrophils but not in T cells nor B cells. As the macrophage and/or neutrophil-specific IL-10-deficient mutants also display the same phenotype, our results suggest that an autocrine loop in monocytes/macrophages is the most probable mechanism for the regulation of an LPS-induced septic shock. In contrast, in an IL-10-regulated T-cell response to Trichuris muris infection, IL-10 acting on T cells or monocytes/macrophages/neutrophils is not critical for the control of the infection. © 2010 Wiley-VCH Verlag GmbH & Co. KGaA.
    Original languageEnglish
    Pages (from-to)443-448
    Number of pages5
    JournalEuropean journal of immunology
    Volume40
    Issue number2
    DOIs
    Publication statusPublished - Feb 2010

    Keywords

    • Conditional gene targeting
    • IL-10 receptor
    • Immune regulation
    • Lipopolysaccharide
    • Trichuris muris

    Fingerprint

    Dive into the research topics of 'Monocytes/macrophages and/or neutrophils are the target of IL-10 in the LPS endotoxemia model'. Together they form a unique fingerprint.

    Cite this