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type 3 innate lymphoid cell-derived lymphotoxin prevents microbiota-dependent inflammation

Cellular & Molecular Immunology 2018年第7期15卷 697-709页

作者： Yuan Zhang Tae-Jin Kim Joanna A Wroblewska Vera Tesic Vaibhav Upadhyay Ralph R Weichselbaum Alexei V Tumanov Hong Tang Xiaohuan Guo Haidong Tang Yang-Xin Fu Department of Pathology University of ChicagoChicagoIL 60637USA Department of Biochemistry and Molecular Biology Korea University College of MedicineSeoul 02841Korea Committee on Immunology Department of PathologyUniversity of ChicagoChicagoIL 60637USA Department of Radiation and Cellular Oncology and The Ludwig Center for Metastasis Research University of ChicagoChicagoIL 60637USA Department of Microbiology Immunology and Molecular GeneticsUniversity of Texas Health Science Center San AntonioSan AntonioTX 78229USA Chinese Academy of Sciences Key Laboratory for Infection and Immunity Institute of BiophysicsChinese Academy of SciencesBeijing 100101China Institute of Immunology Tsinghua University School of MedicineBeijing 100084China Department of Pathology University of Texas Southwestern Medical CenterDallasTX 75390USA

Splenomegaly is a well-known phenomenon typically associated with ***,the underlying cause of this phenotype has not been well ***,the splenomegaly phenotype seen in lymphotoxin(LT)signaling-deficient mice is characterized by increased numbers of splenocytes and splenic ***,as well as the related phenotype of increased lymphocyte counts in non-lymphoid tissues,is thought to result from the absence of secondary lymphoid tissues in LT-deficient *** now present evidence that mice deficient in LTα1β2 or LTβR develop splenomegaly and increased numbers of lymphocytes in non-lymphoid tissues in a microbiota-dependent *** administration to LTα1β2-or LTβR-deficient mice reduces ***,re-derived germ-free Ltbr−/−mice do not exhibit splenomegaly or increased inflammation in non-lymphoid tissues compared to specific pathogen-free Ltbr−/−*** using various LTβ-and LTβR-conditional knockout mice,we demonstrate that retinoic acid-related orphan receptorγT-positive type 3 innate lymphoid cells provide the required active LT signaling to prevent the development of ***,this study demonstrates the importance of LT-mediated immune responses for the prevention of splenomegaly and systemic inflammation induced by microbiota.

关键词： germ-free lymphotoxin microbiota splenomegaly type 3 innate lymphoid cells

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Gut microbiota–SCFAs–interleukin-17A axis orchestrates hepatocellular carcinoma

Gut microbiota–SCFAs–interleukin-17A axis orchestrates hep...

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第十四届全国免疫学学术大会

作者： Chupeng Hu Bingqing Xu Boyuan Liu Yu Jin Jinying Lu Dongju Feng Yun Chen Department of Immunology Key Laboratory of Immune Microenvironment and Disease Nanjing Medical University Jiangsu Key Lab of Cancer Biomarkers Prevention and Treatment Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical University Department of medical imaging and nuclear medicine Medical School of Southeast University Research Center for Clinical Oncology Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research &Nanjing Medical University Affiliated Cancer Hospital

Background: type 3 innate lymphoid cells(ILC3s) are essential for host defense against infection and tissue homeostasis. However, its role in the development of hepatocellular carcinoma(HCC) has not been adequately confirmed. In this study, we investigated the role of short-chain fatty acids(SCFAs) in ILC3 cells, which may modulate HCC ***: The roles of Lactobacillus reuteri and SCFAs in the regulation of cytokine production in liver sorted ILC3s were evaluated, respectively. L. reuteri or wild type mice feces were intragastrically transplanted into HCC mice. We also fed SCFAs to HCC mice through drinking water to assess their role in ILC3 cells in ***: L. reuteri was obviously reduced in the gut microbiota of HCC mice, accompanied by a decrease in acetate levels. Here, rather than propionate and butyrate, acetate was shown to lessen the level of interleukin-17A(IL-17A) produced by ILC3s. Further more, after systematically administering acetate to HCC mice, we found a decrease in IL17A+ILC3s in liver and a slowdown in tumor growth. It was further demonstrated that acetate inhibited ILC3 function probably through inhibiting histone deacetylase(HDAC) due to the similar impact of trichostatin A(a pan-HDAC inhibitor) on ILC3s. It is worth noting that synergistic treatment with acetate and trichostatin A failed to produce an additive effect. Finally, we found that acetate may reduce the production of cytokines in human ***: In this research, acetate was identified to play a key role in regulating the function of ILC3s through the inhibitory activity of its HDACs. This new discovery may be used as a possible therapeutic target for HCC.

关键词： type 3 innate lymphoid cells interleukin-17A hepatocellular carcinoma short-chain fatty acids gut microbiota

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