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Spatial distribution of IL4 controls iNKT cell-DC crosstalk in tumors

Cellular & Molecular Immunology 2020年第5期17卷 496-506页

作者： Lu Wang Zhilan Liu Lili Wang Qielan Wu Xiang Li Di Xie Huimin Zhang Yongdeng Zhang Lusheng Gu Yanhong Xue Ting Yue Gang Liu Wei Ji Haiming Wei Tao Xu Li Bai Division of Life sciences and Medicine Department of Oncology of The First Affiliated HospitalThe CAS Key Laboratory of Innate Immunity and Chronic DiseaseUniversity of Science and Technology of China230027 HefeiChina national Key Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of Sciences100101 BeijingChina School of Life sciences University of Science and Technology of China230027 HefeiChina national Synchrotron Radiation Laboratory University of Science and Technology of China230027 HefeiChina

The spatiotemporal distribution of cytokines orchestrates immune responses in vivo,yet the underlying mechanisms remain to be explored.We showed here that the spatial distribution of interleukin-4(IL4)in invariant natural killer T(iNKT)cells regulated crosstalk between iNKT cells and dendritic cells(DCs)and controlled iNKT cell-mediated T-helper type 1(Th1)responses.The persistent polarization of IL4 induced by strong lipid antigens,that is,α-galactosylceramide(αGC),caused IL4 accumulation at the immunological synapse(IS),which promoted the activation of the IL4R-STAT6(signal transducer and activator of transcription 6)pathway and production of IL12 in DCs,which enhanced interferon-γ(IFNγ)production in iNKT cells.Conversely,the nonpolarized secretion of IL4 induced by Th2 lipid antigens with a short or unsaturated chain was incapable of enhancing this iNKT cell-DC crosstalk and thus shifted the immune response to a Th2-type response.The nonpolarized secretion of IL4 in response to Th2 lipid antigens was caused by the degradation of Cdc42 in iNKT cells.Moreover,reduced Cdc42 expression was observed in tumorinfiltrating iNKT cells,which impaired IL4 polarization and disturbed iNKT cell-DC crosstalk in tumors.

关键词： Spatial distribution Polarization IL4 iNKT DC Crosstalk Tumor

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NKT cells in liver diseases

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Frontiers of Medicine 2018年第3期12卷 249-261页

作者： Shasha Zhu Huimin Zhang Li Bai CAS Key Laboratory of Innate Immunity and Chronic Disease CAS Center for Excellence in Molecular Cell Science School of Life Sciences and Medical Center University of Science and Technology of China Hefei 230027 China Innovation Center for Cell Signaling Network Hefei National Laboratory for Physical Sciences at Microscale Hefei 230027 China

natural killer T cells are innate-like and tissue-resident lymphocytes, which recognize lipid antigens and are enriched in the liver. natural killer T cells play important roles in infections, tumors, autoimmune diseases, and metabolic diseases. In this study, we summarize recent findings on biology of natural killer T cells and their roles in hepatitis B virus and hepatitis C virus infection, autoimmune liver diseases, alcoholic liver disease, nonalcoholic fatty liver disease, and hepatocellular carcinoma. Controversial results from previous studies are discussed, and indicate the dynamic alteration in the role of natural killer T cells during the progression of liver diseases, which might be caused by changes in natural killer T subsets, factors skewing cytokine responses, and intercellular crosstalk between natural killer T cells and CDld-expressing cells or bystander cells.

关键词： natural killer T cells hepatitis B virus and hepatitis C virus infection autoimmune liver diseases alcoholic liverdisease nonalcoholic fatty liver disease hepatocellular carcinoma

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Lactic acid in tumor microenvironments causes dysfunction of NKT cells by interfering with mTOR signaling

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science china(Life sciences) 2016年第12期59卷 1290-1296页

作者： Di Xie Shasha Zhu Li Bai CAS Key Laboratory of lnnate lmmunity and Chronic Disease CAS Center for Excellence in Molecular Cell Science School of Life Sciences and Medical Center University of Science and Technology of China Hefei 230027 China Innovation Center for Cell Signaling Network Hefei National Laboratory for Physical Sciences at Microscale Hefei 230027 China

Cellular metabolism has been shown to regulate differentiation and function of immune cells.Tumor associated immune cells undergo phenotypic and functional alterations due to the change of cellular metabolism in tumor microenvironments.NKT cells are good candidates for immunotherapies against tumors and have been used in several clinical trials.However,the influences of tumor microenvironments on NKT cell functions remain unclear.In our studies,lactic acid in tumor microenvironments inhibited IFNγ and IL4 productions from NKT cells,and more profound influence on IFNγ was observed.By adjusting the pH of culture medium we further showed that,dysfunction of NKT cells could simply be induced by low extracellular pH.Moreover,low extracellular pH inhibited NKT cell functions by inhibiting mammalian target of rapamycin(mTOR) signaling and nuclear translocation of promyelocytic leukemia zinc-finger(PLZF).Together,our results suggest that tumor acidic microenvironments could interfere with NKT cell functions through metabolic controls.

关键词： lactic acid NKT cell IFNγ mTOR PLZF

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Challenges of iNKT cell-based antitumor immunotherapies

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Cellular & Molecular Immunology 2021年第4期18卷 1077-1078页

作者： Huimin Zhang Li Bai Hefei national Laboratory for Physical sciences at Microscale the CAS Key Laboratory of Innate Immunity and Chronic DiseaseSchool of Life SciencesDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiChina

Invariant natural killer T(iNKT)cells are good candidates for antitumor immunotherapies due to their functional advantages and low toxicity.Their promising utility has been exhibited by studies in animal models and cl... 详细信息

关键词： functional Invariant NKT

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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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