<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>12</volume><submitter>Zhang B</submitter><pubmed_abstract>Clonorchiasis caused by &lt;i>Clonorchis sinensis&lt;/i> is a mainly foodborne parasitic disease. It can lead to hepatobiliary duct inflammation, fibrosis, obstructive jaundice, liver cirrhosis, and even cholangiocarcinoma. Interleukin (IL)-10 is an immune-regulatory cytokine which plays an immunosuppressive role during infection. Our previous study found that IL-10 was increased in mice with &lt;i>C. sinensis&lt;/i> infection. However, the role and mechanism of IL-10 playing in hepatobiliary injury induced by &lt;i>C. sinensis&lt;/i> infection remain unknown. Herein, &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> mice and &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> C57BL/6J mice were infected with &lt;i>C. sinensis&lt;/i>. It was found that IL-10 deficiency aggravated biliary hyperplasia and exacerbated periductal fibrosis induced by &lt;i>C. sinensis&lt;/i> infection. Moreover, IL-10 deficiency increased CD4&lt;sup>+&lt;/sup>T cells and CD8&lt;sup>+&lt;/sup>T cells but not macrophages in the liver of mice with infection. There were no apparent differences in Th1 and Treg cells between &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> and &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> mice infected with &lt;i>C. sinensis&lt;/i>. However, the proportion of Th17 cells in CD4&lt;sup>+&lt;/sup>T cells in &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> infected mice was significantly higher than that in &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> infected mice. IL-10 deficiency also enhanced the increase of Th17 cells induced by ESPs stimulation &lt;i>in vitro&lt;/i>. Taken together, our results suggest that IL-10 plays a protective role in hepatobiliary injury in C57BL/6J mice induced by &lt;i>C. sinensis&lt;/i> infection &lt;i>via&lt;/i> inhibiting Th17 cells, which could deepen our understanding of the immunopathology of clonorchiasis.</pubmed_abstract><journal>Frontiers in cellular and infection microbiology</journal><pagination>994838</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9606589</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-10 regulates Th17 response to inhibit hepatobiliary injury caused by &lt;i>Clonorchis sinensis&lt;/i> infection in C57BL/6J mice.</pubmed_title><pmcid>PMC9606589</pmcid><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Liu M</pubmed_authors><pubmed_authors>Yu Q</pubmed_authors><pubmed_authors>Yu G</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Xu J</pubmed_authors><pubmed_authors>Hua H</pubmed_authors><pubmed_authors>Jiang Z</pubmed_authors><pubmed_authors>Koda S</pubmed_authors><pubmed_authors>Zhao Q</pubmed_authors><pubmed_authors>Zheng KY</pubmed_authors><pubmed_authors>Yan C</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Xu YH</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-10 regulates Th17 response to inhibit hepatobiliary injury caused by &lt;i>Clonorchis sinensis&lt;/i> infection in C57BL/6J mice.</name><description>Clonorchiasis caused by &lt;i>Clonorchis sinensis&lt;/i> is a mainly foodborne parasitic disease. It can lead to hepatobiliary duct inflammation, fibrosis, obstructive jaundice, liver cirrhosis, and even cholangiocarcinoma. Interleukin (IL)-10 is an immune-regulatory cytokine which plays an immunosuppressive role during infection. Our previous study found that IL-10 was increased in mice with &lt;i>C. sinensis&lt;/i> infection. However, the role and mechanism of IL-10 playing in hepatobiliary injury induced by &lt;i>C. sinensis&lt;/i> infection remain unknown. Herein, &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> mice and &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> C57BL/6J mice were infected with &lt;i>C. sinensis&lt;/i>. It was found that IL-10 deficiency aggravated biliary hyperplasia and exacerbated periductal fibrosis induced by &lt;i>C. sinensis&lt;/i> infection. Moreover, IL-10 deficiency increased CD4&lt;sup>+&lt;/sup>T cells and CD8&lt;sup>+&lt;/sup>T cells but not macrophages in the liver of mice with infection. There were no apparent differences in Th1 and Treg cells between &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> and &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> mice infected with &lt;i>C. sinensis&lt;/i>. However, the proportion of Th17 cells in CD4&lt;sup>+&lt;/sup>T cells in &lt;i>Il10&lt;sup>+/-&lt;/sup>&lt;/i> infected mice was significantly higher than that in &lt;i>Il10&lt;sup>+/+&lt;/sup>&lt;/i> infected mice. IL-10 deficiency also enhanced the increase of Th17 cells induced by ESPs stimulation &lt;i>in vitro&lt;/i>. Taken together, our results suggest that IL-10 plays a protective role in hepatobiliary injury in C57BL/6J mice induced by &lt;i>C. sinensis&lt;/i> infection &lt;i>via&lt;/i> inhibiting Th17 cells, which could deepen our understanding of the immunopathology of clonorchiasis.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-04T09:41:48.963Z</modification><creation>2025-04-04T09:41:48.963Z</creation></dates><accession>S-EPMC9606589</accession><cross_references><pubmed>36310865</pubmed><doi>10.3389/fcimb.2022.994838</doi></cross_references></HashMap>