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浙江省免疫学会第十次学术大会

作者： Danxiao Wu Yu Shi Cheng Wang Qiaoyun Liu Hanwen Chen Jianhua Liu Lihuang Zhang Yihua Wu Dajing Xia School of public health Zhejiang University School of Medicine Institute of Immunology Zhejiang University School of Medicine State Key Laboratory for Diagnosis and Treatment of Infectious Diseases Collaborative Innovation Center for Diagnosis and Treatment of Infectious DiseaseThe First Affiliated HospitalZhejiang University School of Medicine The Children's Hospital Zhejiang University School of Medicine Department of Clinical Medicine Zhejiang University City College School of Medicine

Myeloid-derived suppressor cells(MDSCs) confer immunosuppressive properties,but their roles in fulminant hepatitis have not been well defined.In this study,we systematically examined the distribution of MDSCs in bone marrow(BM),hver and spleen was determined,and their functional and differentiation status in an acute Fulminant hepatitis mouse model induced by lipopolysaccharide and D-galactosamine(LPS-GaIN).Moreover,the interaction between NKT cells and MDSCs was determined.Our study revealed that BM contained the largest pool of MDSCs during pathogenesis of fulminant hepatitis compared with liver and spleen.MDSCs in liver/spleen expressed higher levels of chemokine receptors such as CCR2,CX3 CR1 and CXCR2.At inflamed tissues such as liver or spleen,activated NKT cells induced differentiation of MDSCs through cell-cell interaction,which markedly dampened the immunosuppressive effects and promoted MDSCs to produce pro-inflammatory cytokines and activate inflammatory cells.Our findings thus demonstrated an unexpected pro-inflammatory state for MDSCs,which is,mediated by the activated NKT cells that precipitated the differentiation and functional evolution of these MDSCs at sites of inflammation.

关键词： myeloid-derived suppressor cell NKT cells Fulminant Hepatitis

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M2-specific reduction of CD1d switches nkt cell-mediated immune responses and triggers metaflammation in adipose tissue

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Cellular & Molecular Immunology 2018年第5期15卷 506-517页

作者： Huimin Zhang Rufeng Xue Shasha Zhu Sicheng Fu Zuolong Chen Rongbin Zhou Zhigang Tian Li Bai CAS Key Laboratory of Innate Immunity and Chronic Disease CAS Center for Excellence in Molecular Cell ScienceSchool of Life Sciences and Medical CenterUniversity of Science and Technology of ChinaHefei 230027China Innovation Center for Cell Signaling Network Hefei National Laboratory for Physical Sciences at MicroscaleHefei 230027China

Metaflammation is responsible for several metabolic syndromes,such as type 2 diabetes.However,the mechanisms by which metabolic disorders trigger metaflammation remain unclear.We identified a cell type-specific downregulation of CD1d expression in M2 macrophages during the progression of obesity prior to the onset of inflammation in visceral adipose tissues.A reduction in CD1d expression influenced the ability of M2 macrophages to present antigens and caused a change in antigen-presenting cells from M2 macrophages to M1 macrophages.With CD1d conditional knockout(KO)mice,we further demonstrated that natural killer T(nkt)cell activation by M2 macrophages inhibited metaflammation and insulin resistance by promoting Th2 responses and M2 polarization in visceral adipose tissues of obese mice,whereas nkt cell activation by M1 macrophages exacerbated metaflammation and insulin resistance by promoting Th1 responses and inhibiting M2 polarization.Our results suggest that an M2-specific reduction of CD1d is an initiating event that switches nkt cell-mediated immune responses and disrupts the immune balance in visceral adipose tissues in obese mice.

关键词： CD1d macrophage metaflammation NKT cells

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nkt cell subsets as key participants in liver physiology and pathology

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Cellular & Molecular Immunology 2016年第3期13卷 337-346页

作者： Keya Bandyopadhyay Idania Marrero Vipin Kumar Department of Medicine University of California San Diego La Jolla CA 92037 USA

Natural killer T （nkt） cells are innate-like lymphocytes that generally recognize lipid antigens and are enriched in microvascular compartments of the liver. NKT cells can be activated by self- or microbial-lipid antigens and by signaling through toll-like receptors. Following activation, NKT cells rapidly secrete pro-inflammatory or anti- inflammatory cytokines and chemokines, and thereby determine the milieu for subsequent immunity or tolerance. It is becoming clear that two different subsets of NKT cells-type I and type II--have different modes of antigen recognition and have opposing roles in inflammatory liver diseases. Here we focus mainly on the roles of both nkt cell subsets in the maintenance of immune tolerance and inflammatory diseases in liver. Furthermore, how the differential activation of type I and type II NKT cells influences other innate cells and adaptive immune cells to result in important consequences for tissue integrity is discussed. It is crucial that better reagents, including CDld tetramers, be used in clinical studies to define the roles of NKT cells in liver diseases in patients.

关键词： CDld lipids liver disease NKT cells

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Immune cells in term and preterm labor

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Cellular & Molecular Immunology 2014年第6期11卷 571-581页

作者： Nardhy Gomez-Lopez Derek StLouis Marcus A Lehr Elly N Sanchez-Rodriguez Marcia Arenas-Hernandez Department of Obstetrics & Gynecology and Immunology & Microbiology Wayne State University Detroit MI USA Perinatology Research Branch NICHD/NIH School of Medicine Wayne State University Detroit MI USA

Labor resembles an inflammatory response that includes secretion of cytokines/chemokines by resident and infiltrating immune cells into reproductive tissues and the maternal/fetal interface. Untimely activation of these inflammatory pathways leads to preterm labor, which can result in preterm birth. Preterm birth is a major determinant of neonatal mortality and morbidity; therefore, the elucidation of the process of labor at a cellular and molecular level is essential for understanding the pathophysiology of preterm labor. Here, we summarize the role of innate and adaptive immune cells in the physiological or pathological activation of labor. We review published literature regarding the role of innate and adaptive immune cells in the cervix, myometrium, fetal membranes, decidua and the fetus in late pregnancy and labor at term and preterm. Accumulating evidence suggests that innate immune cells （neutrophils, macrophages and mast cells） mediate the process of labor by releasing pro-inflammatory factors such as cytokines, chemokines and matrix metalloproteinases. Adaptive immune cells （T-cell subsets and B cells） participate in the maintenance of fetomaternal tolerance during pregnancy, and an alteration in their function or abundance may lead to labor at term or preterm. Also, immune cells that bridge the innate and adaptive immune systems （natural killer T （nkt） cells and dendritic cells （DCs）） seem to participate in the pathophysiology of preterm labor. In conclusion, a balance between innate and adaptive immune cells is required in order to sustain pregnancy; an alteration of this balance will lead to labor at term or preterm.

关键词： B cells cytotoxic T cells dendritic cells macrophages mast cells neutrophils NKT cells parturition preterm delivery regulatory T cells T cells

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Pathogen-expanded CD11b+ regulatory nkt cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Pathogen-expanded CD11b+ regulatory NKT cell feedback inhibi...

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第九届全国免疫学学术大会

作者： Zhengping Jiang Zhubo Chen Yan Gu Yanfang Liu Xiang Zhang Yanmei Han National Key Laboratory of Medical Immunology & Institute of Immunology Second Military Medical University

Natural killer T cells(NKT cells)are not only the effector cells,but also regulator of immune response,which can either promote or suppress cellular immune response through production of different cytokines.However,the subsets of NKT cells with definite phenotype and regulatory function need to be further identified.Furthermore,the mechanisms for NKT cells to regulate immune response remain to be fully elucidated.Here we identified CD11bNKT cells as a new subset of regulatory NKT cells in the mouse models with infection.TCRβNK1.1NKT cells could be categorized to CD1 lb+and CD11bsubsets.During Listeria monocytogenes infection,hepatic CD11bNKT cells were significantly induced and expanded,with peak expansion on day 8.CD11bNKT cells were also expanded significantly in spleen and mesenteric lymph nodes.As compared to CD11bNKT cells,CDllb+NKT cells expressed higher levels of CD27,FasL,B7H1,CD69,and particularly higher level of membrane-bound TGF-β1(mTGF-β1),but produced less TFN-γ,TL-4,TL-10 and TGF-β1.Hepatic CD11bNKT cells suppressed Ag-nonspecific and OVA-specific CD4 and CD8 T cell proliferation through mTGF-β1 both in vitro and in vivo,meanwhile,they did not interfere with activation of CD4 T cells and cytotoxicity of the activated CD8 T cells.Thus,we have identified a new subset of pathogen-expanded CD11bregulatory NKT cells which can feedback inhibit T cell response via cell surface TGF-pi,especially at the late stage of immune response against infection.CD11bregulatory NKT cells may contribute to protect host from pathological injure by preventing immune overactivation.

关键词： NKT cells immune regulation CD11b TGF-β1 Listeria monocytogenes

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Gut commensal bacterial maintain liver innate tolerance for liver regeneration

Gut commensal bacterial maintain liver innate tolerance for ...

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第九届全国免疫学学术大会

作者：吴逊尧陈永艳孙汭田志刚中国科学技术大学免疫学研究所

Backgroud:It has been proposed that products of conmmensal bacteria,such as lipopolysaccharide may play a role in repair of liver hepatocytes after partial(67%)hepateetomy.How commensal bacteria affect the ability of liver regeneration remains elusive.Aim:1.To investigate whether commensal bacteria influence the ability of liver regeneration2.To elusidate the potential mechanism of how commensal bacteria affect liver regeneration Methods:In this study,mice were subjected to a 4 week oral administration of antibiotic combination(A/V/N/M)before subjecting to 70%PHx.At different time point of PHx,liver tissues were collected,weighed.A portion of liver were fixed for PCNA,BrdU/IHC,the remnant liver were weighed and liver lymphocy tes were isolated for FACS.Results:we showed that liver regeneration was impaired in antibiotic water-treated mice.Using various antibiotic treatments,we found that ampicillin-sensitive class of commensal bacteria was response for the impaired liver regeneration.The number and activation of NKT cells were up-regulated in the hepatectomized mice by antibiotic water treatment.Deplete or blockade of CD1d-dependent NKT cells could accelerate the regeneration of hepatocytes.Injection of lipopolysaccharide to induce the tolerance of Kupffer cells could partly promote liver regeneration by reducing the number and activation of NKT cells.Conclusion:Our study reveal the importance of commensal bacteria controling hepatocytes repair by negatively regulating hepatic NKT cells via producing lipopolysaccharide to induce the tolerate of Kupffer cells.

关键词： Commensal bacterial 70%PHx NKT cells Kupffer cells

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