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HMGB1 from Astrocytes Promotes EAE by Influencing the Immune Cell Infiltration-Associated Functions of BMECs in Mice

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Neuroscience Bulletin 2022年第11期38卷 1303-1314页

作者： Junyu Shi Yifan Xiao Na Zhang Mengya Jiao Xuhuan Tang Chan Dai Chenchen Wang Yong Xu Zheng Tan Feili Gong Fang Zheng Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China Key Laboratory of Organ Transplantation Ministry of EducationNHC Key Laboratory of Organ TransplantationKey Laboratory of Organ TransplantationChinese Academy of Medical SciencesWuhan 430030China Department of Pathology and Pathophysiology School of MedicineJianghan UniversityWuhan 430056China

High mobility group box 1(HMGB1)has been reported to play an important role in experimental autoimmune encephalomyelitis(EAE).Astrocytes are important components of neurovascular units and tightly appose the endothelial cells of microvessels by their perivascular endfeet and directly regulate the functions of the blood-brain barrier.Astrocytes express more HMGB1 during EAE while the exact roles of astrocytic HMGB1 in EAE have not been well elucidated.Here,using conditional-knockout mice,we found that astrocytic HMGB1 depletion decreased morbidity,delayed the onset time,and reduced the disease score and demyelination of EAE.Meanwhile,there were fewer immune cells,especially pathogenic T cells infiltration in the central nervous system of astrocytic HMGB1 conditional-knockout EAE mice,accompanied by up-regulated expression of the tight-junction protein Claudin5 and down-regulated expression of the cell adhesion molecules ICAM1 and VCAM1 in vivo.In vitro,HMGB1 released from astrocytes decreased Claudin5 while increased ICAM1 and VCAM1 expressed by brain microvascular endothelial cells(BMECs)through TLR4 or RAGE.Taken together,our results demonstrate that HMGB1 derived from astrocytes aggravates EAE by directly influencing the immune cell infiltration-associated functions of BMECs.

关键词： HMGB1 Astrocytes Experimental autoimmune encephalomyelitis Blood-brain barrier

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KIR2DL2/C1 is a Risk Factor for Chronic Infection and Associated with Non-response to PEG-IFN and RBV Combination Therapy in Hepatitis C Virus Genotype 1b Patients in China

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Virologica Sinica 2018年第4期33卷 369-372页

作者： Song Hu Fahu Yuan Lingyan Feng Fang Zheng Feili Gong Hanju Huang Binlian Sun Medical College Jianghan University Department of Immunology School of Basic MedicineTongji Medical College Huazhong University of Science and Technology Department of Pathogen Biology Tongji Medical CollegeHuazhong University of Science and Technology

Dear Editor,Natural killer(NK)cells are lymphocytes that play important roles in the host defense against hepatitis C virus(HCV)infection.Killer cell immunoglobulin-like receptors(KIRs)are a group of regulatory molecules expressed on NK cells and a subset of T cells(Parham 2005).Ligands for KIRs are human leukocyte antigen(HLA)class Ⅰ molecules,and HLA-C1 is a ligand for the

关键词：丙肝病毒风险因素联合治疗感染遗传型反应中国免疫球蛋白

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Indoleamine 2,3-dioxygenase and regulatory dendritic cells contribute to the allograft protection induced by infusion of donor-specific splenic stromal cells

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Cellular & Molecular Immunology 2011年第1期8卷 31-40页

作者： Li Liu Lihua Duan Min gong Hong Dai Quan gong Fang Zheng Zheng Tan Congyi Wang Feili Gong Min Fang Laboratory of Transplantation Department of ImmunologyTongji Medical College of Huazhong University of Science and TechnologyWuhanChina The Center for Biomedical Research Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

It has been reported that splenic stromal cells(SSCs)are capable of directly supporting the development of CD11c ^(lo)CD45RB^(+) IL-10-producing dendritic cells(DCs)from lineage-negative c-kit^(+) progenitor cells in the absence of exogenous cytokines.In vitro,DCs that differentiate on stromal cells suppress mixed leukocyte reaction responses and induce primary alloreactive CD4^(+) T cells to differentiate into IL-10-producing Tr1 cells.However,the precise mechanisms by which these SSCs exert their regulatory functions in vivo remain undefined.Furthermore,their possible contribution to the development of allograft transplantation tolerance has yet to be examined.Here,we have used both murine skin and cardiac allograft transplantation models to explore whether in vivo alloresponses can be regulated by infusion with donor-derived SSCs and to investigate the possible mechanisms by which SSCs exert regulatory effects to prevent allograft rejection.We show that intravenous SSC infusion prolonged murine skin allograft survival.The prolonged graft survival is associated with augmentation of the generation of regulatory DC subsets and CD4^(+) CD25^(+) Foxp3^(+) regulatory T cells(Tregs),as well as upregulation of the production of suppressive cytokines IL-10 and transforming growth factor(TGF)-b.Moreover,we found that indoleamine 2,3-dioxygenase and SSC-derived regulatory DCs contribute to allograft protection by infusion of donor-specific SSCs.Our data suggest that donor-derived SSCs could be used as a therapeutic target to promote transplantation tolerance.

关键词： dendritic cell indoleamine 2,3-dioxygenase splenic stromal cell transplantation

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Gene Delivery of SOCS3 Protects Mice from Lethal Endotoxic Shock

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Cellular & Molecular Immunology 2005年第5期2卷 373-377页

作者： Min Fang Hong Dai Guang Yu Feili Gong Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China These authors contributed equally to this work

Suppressor of cytokine signaling 3 （SOCS3） was reported as a feedback inhibitor of cytokine receptor signaling by inhibiting the JAK-STAT signal transduction pathway. We sought to test the anti-endotoxic septic shock effect of liposome mediated gene delivery of SOCS3 in a lethal endotoxic shock mouse model. BALB/c mice were injected intraperitoneally with 200μg pcDNA3.1-SOCS3 cationic liposomes, while pcDNA3.1-IL-10 and empty vector as positive and negative control respectively. Forty-eight hours after gene delivery, mice were challenged with 4 μg of E.coli 0127：B8 LPS and 18 mg D-GaIN administered i.p. 90 min later, serum TNF-α level was determined. Survival over the next 48 h was evaluated. Peritoneal macrophages from survival mice were stimulated in vitro with 1 μg/ml LPS for 18 h, and the supernatants were harvested for determination of the amount of TNF-α. We found that gene delivery of SOCS3 significantly increase the mouse survival rate from 27.8 ± 9.6% of control group to 61.1 ± 9.6% （p 〈 0.01）. In comparison with control group （218 ± 13 pg/ml） and sham delivery group （219 ± 22 pg/ml）, gene delivery of SOCS3 reduced the level of serum TNF-α （68 ± 9 pg/ml） significantly （p 〈 0.01）. Furthermore, gene delivery of SOCS3 displayed the capacity of prevention of tolerance of peritoneal macrophages to LPS. These findings suggest that gene delivery of SOCS3 mediated by liposome is a promising approach for endotoxic septic shock treatment. Cellular ＆ Molecular Immunology.

关键词： gene delivery SOCS3 endotoxic septic shock

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Construction and Identification of a Human Liver Specific MicroRNA Eukaryotic Expression Vector

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Cellular & Molecular Immunology 2007年第6期4卷 473-477页

作者： Shanshan Chen Ming Ni Bing Yu Tingting Lv Mengji Lu Feili Gong Department of Pathogenic Biology Tongji Medical College of Huazhong University of Science ＆ Technology Wuhan 430030 China Department of Infectious Diseases Tongji Hospital Tongji Medical College of Huazhong University of Science ＆ Technology Wuhan 430030 China Department of Immunology Tongji Medical College of Huazhong University of Science ＆ Technology Wuhan 430030 China

MiR-122 is one of the non-coding RNAs which showed its effects on the lipo-metablism, virus infection and HCC forming through regulation of liver gene expression. Its eukaryotic expression vector was constructed by using pSuper which was widely applied in the siRNA expression. The precursor of human miR-122 gene was amplified by polymerase chain reaction （PCR） from the human genomic DNA. The positive clones were screened by PCR and restriction enzyme digestion. The new expression vector of miR-122 was named pHsa-m122. PHsa-m122 and its controls were transfected to HepG2 cells. The miR-122 expression activity was evaluated by GFP122i sensor reporter plasmid through fluorescence detection and Western blot. It was shown that the fluorescence intensity of GFP122si and pHsa-m122 co-transfection group was weaker than that of the controls, so the functional activity of expressed miR-122 was detected. When HepG2 cells were co-transfected with HBV1.3 and pHsa-m122 plasmids, the results showed miR-122 may down-regulate the gene expression of HBV. The human liver specific microRNA eukaryotic expression vector of miR-122 was constructed successfully, which may facilitate further study of its function in the development of liver virus infection diseases and HCC. Cellular ＆ Molecular Immunology.

关键词： miRNA miR-122 eukaryotic expression vector pSuper

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Plasmacytoid dendritic cell deficiency in neonates enhances allergic airway inflammation via reduced production of IFN-α

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Cellular & Molecular Immunology 2020年第5期17卷 519-532页

作者： Min Wu Liuchuang Gao Miao He Hangyu Liu Han Jiang Ketai Shi Runshi Shang Bing Liu Shan Gao Hebin Chen Feili Gong Erwin WGelfand Yafei Huang Junyan Han Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Respiratory Medicine Zhongnan Hospital of Wuhan UniversityWuhanChina Department of Respiratory Diseases Wuhan Central HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Pulmonary Medicine Wuhan Children’s HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Division of Cell Biology Department of PediatricsNational Jewish HealthDenverCOUSA Department of Pathogen Biology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina

Allergic asthma,a chronic inflammatory airway disease associated with type 2 cytokines,often originates in early life.Immune responses at an early age exhibit a Th2 cell bias,but the precise mechanisms remain elusive.Plasmacytoid dendritic cells(pDCs),which play a regulatory role in allergic asthma,were shown to be deficient in neonatal mice.We report here that this pDC deficiency renders neonatal mice more susceptible to severe allergic airway inflammation than adult mice in an OVA-induced experimental asthma model.Adoptive transfer of pDCs or administration of IFN-αto neonatal mice prevented the development of allergic inflammation in wild type but not in IFNAR1−/−mice.Similarly,adult mice developed more severe allergic inflammation when pDCs were depleted.The protective effects of pDCs were mediated by the pDC-/IFN-α-mediated negative regulation of the secretion of epithelial cell-derived CCL20,GM-CSF,and IL-33,which in turn impaired the recruitment of cDC2 and ILC2 cells to the airway.In asthmatic patients,the percentage of pDCs and the level of IFN-αwere lower in children than in adults.These results indicate that impairment of pDC-epithelial cell crosstalk in neonates is a susceptibility factor for the development of allergeninduced allergic airway inflammation.

关键词： Neonate Plasmacytoid Dendritic Cells Allergic airway inflammation IFN-α Airway epithelial cells

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Soluble Mouse B7-H3 Down-Regulates Dendritic Cell Stimulatory Capacity to Allogenic T Cell Proliferation and Production of IL-2 and IFN-γ

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Cellular & Molecular Immunology 2006年第3期3卷 235-240页

作者： Junfa Xu Baojun Huang Ping Xiong Wei Feng Yong Xu Min Fang Fang Zheng Feili Gong Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430030 China Department of Clinical Immunology Guangdong Medical College Zhanjiang Guangdong 524023 China Department of Immunology Anhui Medical University Hefei Anhui 230032 China

B7-H3 is a recently identified member of the B7 gene family. Its ubiquitous expression in both lymphoid and nonlymphoid tissues suggests that it could play an important role in the maintenance of self-tolerance. However, the exact function of B7-H3 is still elusive. The purpose of current study is to demonstrate the possible function of soluble mouse B7-H3 for prevention of DC-mediated T cell activation. For this purpose, we established a soluble mouse B7-H3 fusion protein （mB7h3-hIg） eukaryotic expression vector （pmB7h3-hIg） with a C-terminal human IgG1 Fc. A C57BL/6 （B6）-derived dendritic cell line （DC2.4 cells） was used for the establishment of stable transfectants for generation of soluble mB7h3-hIg. Ectopic mB7h3-hIg expression was confirmed by RT-PCR, Western blot and ELISA analyses. A 49.7 kD protein was detected by Western blot from DC2.4 cells transfected with pmB7h3-hlg. It was found that soluble mB7h3-hIg expression has no effect on cell cycling and apoptosis and the expression of CD80 and CD86 of the DC2.4 cells. However, ectopic soluble mB7h3-hIg expression was found to significantly affect the allo-stimulatory capability for DC2.4 cells. DC2.4 cells expressing soluble mB7h3-hIg showed a significant reduced allo-stimulatory capability as compared with the controls determined by MLC. Further studies revealed that soluble mB7h3-hIg could also inhibit IL-2 and IFN-γ, production of allogenic T cells. These results suggested a great potential of soluble B7-H3 for treatment of graft rejection and autoimmume disease. Cellular ＆ Molecular Immunology. 2006;3（3）：235-240.

关键词： B7-H3 dendritic cell T cell proliferation IL-2 IFN-γ

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IL-10 Gene Modified Dendritic Cells Inhibit T Helper Type 1-Mediated Alloimmune Responses and Promote Immunological Tolerance in Diabetes

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Cellular & Molecular Immunology 2008年第1期5卷 41-46页

作者： Huifen Zhu Wenhong Qiu Ping Lei Wei Zhou Xue Wen Fengrong He Li Li Hong Dai Guanxin Shen Feili Gong Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Medicine and Life Science College of Jianghan University Wuhan 430056 China These authors contributed equally to this work

Dendritic cells （DCs） have the potency to regulate the outcome of autoimmunity through the modulation of immune responses. The induction of antigen specific tolerance is critical for prevention and treatment of allograft rejection. In the present Study, we transfected IL-10 gene into DCs and investigated their effect on inhibition of lymphocyte activity in vitro and induction of immune tolerance on islet allograft in mice. An IDDM C57BL/6 mouse model was induced by streptozotocin. The islet cells isolated from the BALB/c mice were transplanted into the kidney capules of the model mice followed by injection of IL-10 modified DCs （mDCs）. The results showed that mDCs could significantly inhibit T lymphocyte proliferation mediated by allotype cells and induce its apoptosis, whereas, unmodified DCs （umDCs） could promote the murine lymphocyte proliferation markedly. The injection of mDCs could prolong the survival of allotype islet transplanted IDDM mice. The average plasma glucose （PG） level in mDCs treated mice returned to normal within 3 days and lasted for about 2 weeks. The rejection response in control mice occurred for 5 days after transplantation. The level of IFN-γ was lower while IL-4 was higher in mDCs treated mice than that in umDCs treated mice, which indicated that Thl/Th2 deviation occurred. Our studies suggest that IL-10 gene modified DCs can induce the immune tolerance to islet graft and prolong survival of the recipients by the inhibiting of T cell proliferation in allotype mice. Cellular ＆ Molecular Immunology.

关键词： IL-10 dendritic cell IDDM islet transplantation immune tolerance

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同种器官移植免疫耐受的研究进展

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中华器官移植杂志 1998年第3期19卷 129-129页

作者：龚非力同济医科大学武汉430030

虽然同种组织及器官移植已有近半个世纪的历史，但移植后的排斥反应仍是亟待解决的关键问题。如何有效地诱导产生免疫耐受，成为移植免疫学研究领域的重要课题，迄今已取得如下进展：一、主动免疫诱导同种移植免疫耐受乃通过接种具有移... 详细信息

虽然同种组织及器官移植已有近半个世纪的历史，但移植后的排斥反应仍是亟待解决的关键问题。如何有效地诱导产生免疫耐受，成为移植免疫学研究领域的重要课题，迄今已取得如下进展：一、主动免疫诱导同种移植免疫耐受乃通过接种具有移植物抗原特异性的Ｔ细胞疫苗（ＴＣＶ...

关键词：同种移植器官移植免疫耐受性

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IL-33 promotes the development of psoriasis in an IL-17 independent manner

IL-33 promotes the development of psoriasis in an IL-17 inde...

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第十三届全国免疫学学术大会

作者： Fanfan Zeng Jie Mao Yong Xu Ping Xiong Zheng Tan Feili Gong Fang Zheng Department of Immunology School of Basic MedicineTongji Medical CollegeHuazhong University of Science and Technology

Background: IL-33 is constitutively highly expressed in skin tissue. Psoriasis is a common autoimmune disease of the skin. The role of IL-33 in the development of psoriasis has rarely been studied.Objective: To study the roles of IL-33 in the development of psoriasis Methods: 1. The appropriate data set in GEO database was analyzed. 2. Western blot and IHC were performed using clinical samples. 3. 5% of imiquimod was applied to induce a psoriasis-like skin inflammation. The disease severity was assessed according to the PASI scoring standard. The lesion and non-lesion skin were subject to western blot, HE staining, immune cells analyzation by flow cytometry. mIL-33 was intradermally administered to WT and IL-17-/-mice to observe the inflammation progression. Immunofluorescence was carried out to confirm the main source of IL-33 and prominent ST2+ cells in skin. 4. Primary keratinocytes were stimulated by homogenate of skin lesions to detect the release of IL-33. IL-33 stimulation was performed to detect the expression of cytokines and chemokines related to psoriasis.Results: IL-33 mRNA and protein in lesion skin was higher than non-lesion skin in psoriasis patient and mice. IL-33 or ST2 gene knockout decreased the clinical scoring accompanied with remising in stratum corneum thickening, parakeratosis, inflammatory infiltration, vasodilation and Munro microabscess. The number of Th17, IL-17+ γδT cells, neutrophils and mast cells decreased in the lesion skin of IL-33 knockout mouse. Subcutaneous administration of IL-33 aggravated the severity of psoriasis-like inflammation and increased local neutrophil infiltration, and this process was independent on IL-17. IL-33 and ST2 were mainly expressed by keratinocyte. Psoriatic lesion homogenate promoted the expression and release of IL-33 by primary keratinocyte. IL-33 alone stimulation promoted gene expression of cytokines and chemokines associated with psoriasis.Conclusion: IL-33 promotes the development of psoriasis in keratinocyte mediated and IL-17 independent manne

关键词： IL-33 keratinocyte neutrophils psoriasis

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