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 language | English |
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Pages (from-to) | 443-448 |
Number of pages | 5 |
Journal | European journal of immunology |
Volume | 40 |
Issue number | 2 |
DOIs | |
Publication status | Published - Feb 2010 |
Keywords
- Conditional gene targeting
- IL-10 receptor
- Immune regulation
- Lipopolysaccharide
- Trichuris muris