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Immune response to inactivated bacterial vector carrying the recombinant K39 antigen of Leishmania infantum in mice

Asian Pacific Journal of Tropical Biomedicine 2024年第5期14卷 199-206页

作者： Lucelina S.Araújo Bruno B.Silva Eduarda N.F.N.Santos Arnaldo S.Bezerra Samuel S.Frota Assis R.Montenegro Eridan O.P.T.Florean Maurício Fvan Tilburg Maria Izabel F.Guedes Laboratory of Biotechnology and Molecular Biology Northeast Biotechnology NetworkState University of CearáFortalezaBrazil Faculty of Veterinary Medicine State University of CearáFortalezaBrazil

Objective:To evaluate the immunological response elicited by an inactivated bacterial vector carrying the K39 antigen of Leishmania infantum,and a purified antigen.Methods:Mice were subjected to the following treatments:(1)Purified recombinant K39(rK39)protein at a 20μg dose with complete Freund’s adjuvant;(2)Inactivated Escherichia coli(BL21 DE3)carrying the K39 protein at an equivalent total protein content of 200μg;(3)Inactivated bacteria lacking the K39 protein;(4)Non-immunized control animals.Serological monitoring was performed.All groups were challenged by intraperitoneal injection of 10^(7) Leishmania infantum promastigotes.After euthanasia,the liver and spleen were collected to analyze the levels of TNF,IFN-γ,IL-12,IL-4,and IL-10.Results:Mice immunized with purified rK39 or the inactivated bacterial vector carrying the K39 antigen of Leishmania infantum showed a long-lasting immune response with high levels of polyclonal antibodies specifically recognizing the recombinant proteins.the IgG1 subclass was the predominant immunoglobulin;however,the induction of IgG2a and the profile of cytokines produced were indicative of the induction of a mixed-type response.Conclusions:the inactivated bacterial vector carrying the K39 antigen,as well as the purified antigen can induce a long-lasting immune response in immunized mice,predominantly favouring a th2 profile response.

关键词： Visceral leishmaniasis K39 Inactivated bacterial vector Vaccine Immune response th1 th2 Leishmania infantum

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萆薢渗湿汤对急性湿疹小鼠模型th1/th2/th22免疫功能的影响

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山西中医药大学学报 2024年第3期25卷 251-255页

作者：李丹周琪琪郑恺俐贾颖山西中医药大学山西晋中030619

目的:探讨萆薢渗湿汤对急性湿疹小鼠模型的治疗效果及对th细胞介导的免疫功能相关机制的研究。方法:将30只KM小鼠随机分为空白组(Normal)、模型组(Model)和萆薢渗湿汤治疗组(BXSST),采用2,4-二硝基氯苯(DNCB)建立急性湿疹小鼠模型。造... 详细信息

目的:探讨萆薢渗湿汤对急性湿疹小鼠模型的治疗效果及对th细胞介导的免疫功能相关机制的研究。方法:将30只KM小鼠随机分为空白组(Normal)、模型组(Model)和萆薢渗湿汤治疗组(BXSST),采用2,4-二硝基氯苯(DNCB)建立急性湿疹小鼠模型。造模成功后,治疗组给予1.3 g/ml萆薢渗湿汤0.2 ml/只灌胃,空白组与模型组给予等量生理盐水灌胃。HE染色观察小鼠耳部组织的病理变化,ELISA检测小鼠血清中白细胞介素22(IL-22)、白细胞介素-4(IL-4)和白细胞介素-2(IL-2)的表达水平。结果:HE染色病理切片显示与模型组比较,萆薢渗湿汤组表皮棘层厚度明显降低,组织内炎症细胞浸润减少;与空白组相比,模型组小鼠血清中IL-2表达降低(P1),IL-4、IL-22水平均明显升高(P1);与模型组比较,萆薢渗湿汤治疗组中IL-2表达升高(P1),IL-4与IL-22水平降低(P<0.05)。结论:萆薢渗湿汤可通过调节IL-2、IL-4及IL-22细胞因子的水平,来改善小鼠急性湿疹的症状。

关键词：萆薢渗湿汤急性湿疹 th1 th2 th22

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NR4A1 agonist cytosporone B attenuates neuroinflammation in a mouse model of multiple sclerosis

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Neural Regeneration Research 2022年第12期17卷 2765-2770页

作者： Hai-Zhen Yu Bing-Qing Zhu Lin Zhu Shuo Li Li-Mei Wang Department of Neurology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenan ProvinceChina

Nuclear receptor subfamily 4 group A1(NR4A1)is an orphan nuclear receptor,which is expressed in the majority of cells.NR4A1 expression in peripheral blood mononuclear cells is low during the preclinical stage of multiple sclerosis.Knockout of the Nr4a1 gene in mice can aggravate the symptoms of experimental autoimmune encephalomyelitis(EAE),which is an animal model of multiple sclerosis.In this study,we intragastrically administered the NR4A1 agonist cytosporone B(Csn-B)to mice after inducing EAE.After treatment with Csn-B,the clinical symptoms in the EAE mice were substantially attenuated compared with that in PBS-treated control mice.the percentages of CD4+T cells and F4/80+cells in the central nervous system were decreased.In addition,interferon-γand interleukin-17 production by proinflammatory th1/th17 cells in the central nervous system and interferon-γlevels in splenocytes were decreased after Csn-B treatment.these findings suggest that the NR4A1 agonist Csn-B can alleviate nerve injury after EAE induction,and,therefore,may be useful as a potential treatment for multiple sclerosis.

关键词： cytosporone B(Csn-B) experimental autoimmune encephalomyelitis macrophages microglia multiple sclerosis NR4A1 agonist NR4A1 th1 th17 treatment

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Caraway extract alleviates atopic dermatitis by regulating oxidative stress,suppressing th2 cells,and upregulating th1 cells in mice

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Asian Pacific Journal of Tropical Biomedicine 2022年第10期12卷 421-429页

作者： Fardin Khajepour Mohammad Reza Zangouyee Arezu Khosravimashizi Ali Afgar Vahideh Abdollahi Shahriar Dabiri Reza Nosratabadi Department of Medical Immunology Afzalipour Faculty of MedicineKerman University of Medical SciencesKermanIran Research Center for Hydatid Disease in Iran Afzalipour Faculty of MedicineKerman University of Medical SciencesKermanIran Student Research Committee Afzalipour Faculty of MedicineKerman University of Medical SciencesKermanIran Department of Animal Biology Kharazmi UniversityTehranIran Department of Pathology Afzalipour Faculty of MedicineKerman University of Medical SciencesKermanIran Pathology and Stem Cells Research Center Afzalipour Faculty of MedicineKerman University of Medical SciencesKermanIran Gastroenterology and Hepathology Research Center Institute of Basic and Clinical Physiology SciencesKerman University of Medical SciencesKermanIran

Objective:To explore the anti-inflammatory and antioxidant effects of caraway on atopic dermatitis(AD)in mice.Methods:AD was induced in two stages,including sensitization and challenge with the application of 2,4 dinitrochlorobenzene 2% and 0.2%,respectively.Clinical symptoms and histological analysis of the skin were assessed.the effects of caraway on oxidant/antioxidant parameters as well as th1-and th2-related cytokines were also evaluated.Results:Caraway reduced the severity of dermatitis in AD-induced mice,as evidenced by significant inhibition of th2-related cytokines(IL-4 and IL-13)and increased th1-related cytokine(IFN-γ).Additionally,treatment with caraway significantly increased superoxide dismutase and catalase activity and decreased the malondialdehyde level in the serum of AD mice.Furthermore,caraway inhibited the differentiation of th2 cells while favoring th1 cell differentiation in the spleen via regulating their master transcription factors GATA3 and T-bet.Conclusions:Caraway could improve AD autoimmune responses and could be considered a potential candidate to treat AD disease.

关键词： Carum carvi L. Caraway Atopic dermatitis 2,4 dinitrochlorobenzene th2 th1 Oxidative stress

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th1 cytokines promote T-cell binding to antigen-presenting cells via enhanced hyaluronan production and accumulation at the immune synapse

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Cellular & Molecular Immunology 2010年第3期7卷 211-220页

作者： Paul L Bollyky Stephen P Evanko Rebecca P Wu Susan Potter-Perigo S Alice Long Brian Kinsella Helena Reijonen Kelly Guebtner Brandon Teng Christina K Chan Kathy R Braun John A Gebe Gerald T Nepom thomas N Wight Benaroya Research Institute SeattleWAUSA

Hyaluronan(HA)production by dendritic cells(DCs)is known to promote antigen presentation and to augment T-cell activation and proliferation.We hypothesized that pericellular HA can function as intercellular‘glue’directly mediating T cell–DC binding.Using primary human cells,we observed HA-dependent binding between T cells and DCs,which was abrogated upon pre-treatment of the DCs with 4-methylumbelliferone(4-MU),an agent which blocks HA synthesis.Furthermore,T cells regulate HA production by DCs via T cell-derived cytokines in a T helper(th)subset-specific manner,as demonstrated by the observation that cell-culture supernatants from th1 but not th2 clones promote HA production.Similar effects were seen upon the addition of exogenous th1 cytokines,IL-2,interferon c(IFN-c)and tumor necrosis factor a(TNF-a).the critical factors which determined the extent of DC–T cell binding in this system were the nature of the pre-treatment the DCs received and their capacity to synthesize HA,as T-cell clones which were pre-treated with monensin,added to block cytokine secretion,bound equivalently irrespective of their th subset.these data support the existence of a feedforward loop wherein T-cell cytokines influence DC production of HA,which in turn affects the extent of DC–T cell binding.We also document the presence of focal deposits of HA at the immune synapse between T-cells and APC and on dendritic processes thought to be important in antigen presentation.these data point to a pivotal role for HA in DC–T cell interactions at the IS.

关键词： dendritic cell hyaluronan immune synapse pericellular matrix th1

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MAP3K2 augments th1 cell differentiation via IL-18 to promote T cell-mediated colitis

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Science China(Life Sciences) 2021年第3期64卷 389-403页

作者： Ningbo Wu Dongping Chen Hongxiang Sun Jianmei Tan Yao Zhang Tianyu Zhang Yuheng Han Hongzhi Liu Xinxing Ouyang Xiao-Dong Yang Xiaoyin Niu Jie Zhong Zhengting Wang Bing Su Shanghai Institute of Immunology Department of Immunology and Microbiologyand Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of EducationShanghai JiaoTong University School of MedicineShanghai 200025China Shanghai JiaoTong University School of Medicine-Yale Institute for Immune Metabolism Shanghai JiaoTong University School of MedicineShanghai 200025China Department of Gastroenterology Ruijin HospitalShanghai JiaoTong University School of MedicineShanghai 200025China

T cell-mediated immunity in the intestine is stringently controlled to ensure proper immunity against pathogenic microbes and to prevent autoimmunity,a known cause of inflammatory bowel disease.However,precisely how T cells regulate intestine immunity remains to be fully understood.In this study,we found that mitogen-activated protein kinase kinase kinase 2(MAP3K2)is required for the CD4^(+)T cell-mediated inflammation in the intestine.Using a T cell transfer colitis model,we found that MAP3K2-deficient naïve CD4^(+)T cells had a dramatically reduced ability to induce colitis compared to wild type T cells.In addition,significantly fewer IFN-γ-but more IL-17A-producing CD4^(+)T cells in the intestines of mice receiving MAP3K2-deficient T cells than in those from mice receiving wild type T cells was observed.Interestingly,under well-defined in vitro differentiation conditions,MAP3K2-deficient naïve T cells were not impaired in their ability to differentiate into th1,th17 and Treg.Furthermore,the MAP3K2-regulated colitis severity was mediated by th1 but not th17 cells in the intestine.At the molecular level,we showed that MAP3K2-mediated th1 cell differentiation in the intestine was regulated by IL-18 and required specific JNK activation.Together,our study reveals a novel regulatory role of MAP3K2 in intestinal T cell immunity via the IL-18-MAP3K2-JNK axis and may provide a novel target for intervention in T cell-mediated colitis.

关键词： MAP3K2 IL-18 th1 T cell immunity colitis

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th17 cells and IL-17 are involved in the disruption of vulnerable plaques triggered by short-term combination stimulation in apolipoprotein E-knockout mice

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Cellular & Molecular Immunology 2013年第4期10卷 338-348页

作者： Tian Ma Qi Gao Faliang Zhu Chun Guo Qun Wang Fei Gao Lining Zhang Department of Immunology Shandong University School of Medicine and Jinan China Key Laboratory of Cardiovascular Remodeling and Function Research Qilu Hospital Shandong University .linan China

Considerable evidence indicates that type 1 T helper （th 1）- and th 17-mediated immune responses promote the formation of atherosclerotic plaques while that CD4＋CD25＋Foxp3＋ regulatory T cells （Tregs） have a protective effect. However, the functions of diverse CD4＋ lymphocyte subsets in plaque rupture remain poorly understood because of a shortage of satisfactory plaque rupture models. Here, we established a murine model of atherosclerotic plaque rupture using a high-fat diet and collar placement on the carotid artery, and triggered plaque rupture by short-term stimulation with a combination of lipopolysaccharide, phenylephrine injection and cold in apolipoprotein E-knockout （ApoE-/-） mice. We investigated the associations between thl cells, th17 cells and Tregs and plaque rupture by PCR, flow cytometry, ELISA and immunohistochemistry. In total, 75% （18/24） of vulnerable plaques, but no stable plaques, showed rupture characteristics. the proportion of th17 cells was increased among splenocytes after treatment, but the changes in the levels of thl ceils and Tregs were not related to rupture. Furthermore, the treatment resulted in high levels of interleukin- 17 （IL-17） in the serum and in the region of plaque rupture, in vitro, IL-17 increased the level of apoptosis, a major factor associated with plaque rupture, in cultured murine vascular smooth muscle cells. th17 cells and IL-17 may be involved in the disruption of vulnerable plaques triggered by short-term stimulation with lipopolysaccharide, phenylephrine injection and cold in ApoE-/-mice.

关键词： atherosclerosis mice plaque rupture th1 th17

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Curcumin regulated shift from th1 to th2 in trinitrobenzene sulphonic acid-induced chronic colitis

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Acta Pharmacologica Sinica 2006年第8期27卷 1071-1077页

作者： Ming ZHANG~(3,4) Chang-sheng DENG~1 Jia-ju ZHENG~2 Jian XIA~1 ~1Department of Gastroenterology,Zhongnan Hospital of Wuhan University,Wuhan 430071,China ~2Municipal Hospital of Suzhou,Suzhou 215008,China ~3Department of Gastroenterology,Drum Tower Hospital of Nanjing,Nanjing 210008,China Department of Gastroenterology Drum Tower Hospital of Nanjing Nanjing China Department of Gastroenterology Zhongnan Hospital of Wuhan University Wuhan China Municipal Hospital of Suzhou Suzhou China

Aim:To investigate the therapeutic effects of curcumin（Cur）on trinitrobenzenesulphonic acid（TNBS）-induced colitis and the effects of Cur on the balance ofth1/th2 cytokines.Methods:Colitis was induced by TNBS and treated with Cur(30mg.kg-1·d-1,ip),dexamethasone(Dex,2 mg·kg-1·d-1),or Cur plus dexamethasone(Cur+Dex,30 mg.kg-1·d-1Cur ip+2 mg.kg-1·d-1Dex,ip).mRNA in colon mucosawere detected by real-time quantitative polymerase chain reaction.Intracellularcytokines were detected by flow cytometry and concentrations of cytokines insera were detected by enzyme-linked immunosorbent analysis.Results:Both Curand Dex improved body weight loss,ameliorated histological images and de-creased macroscopic score and myeloperoxidase activity.Cur decreased the ex-pression of th1 cytokines（IL-12,IFN-γ,TNF-α,IL-1）and increased the expres-sion of th2 cytokines（IL-4 and IL-10）in colon mucosa.Cur also increased theproportion of IFN-γ/IL-4 in splenocytes and circulation.Dex and Cur+Dex de-creased the expression of th1 cytokines but could not increase the expression ofth2 cytokines and the proportion of IFN-γ/IL-4.Conclusion:Cur exerted thera-peutic effects on colitis by regulating the shift from th1 to th2.

关键词： colitis curcumin IL-4 IL-12 th1 th2

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CTLA4 Silencing with siRNA Promotes Deviation of th1/th2 in Chronic Hepatitis B Patients

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Cellular & Molecular Immunology 2009年第2期6卷 123-127页

作者： Yongsheng Yu Hao Wu Zhenghao Tang Guoqing Zang Department of Infectious Diseases. Sixth People＇s Hospital Shanghai Jiaotong University Shanghai 200233 China

To determine whether RNA interference （RNAi） could block cytotoxic T-lymphocyte antigen 4 （CTLA4） in human lymphocytes in vitro and promote IFN-T and IL-2 secretions, three small interfering RNAs （siRNAs） were selected based on target specificity sequences of human CTLA4 and transfected into human lymphocytes of chronic HBV patients. As a result, the expression of human CTLA4 mRNA was efficiently suppressed by all the three siRNAs. Compared with negative control （siRNA-co）, siRNA-1 inhibited the expression of CTLA4 most efficiently and was used in the further study. the expressions of IFN-γ and IL-2 were upregulated and the level of IL-4 was almost unchanged in lymphocytes transfected with siRNA-1 compared with the blank control. these results indicated that siRNA-1 led to IFN-γ and IL-2 secretions, which is a main response of th1/th2. In a conclusion, RNAi significantly suppressed the expression of human CTLA4 mRNA in human lymphocytes in vitro, and could induce th1/th2 response. It could be a new therapeutic strategy for chronic HBV infection.

关键词： CTLA4 siRNA lymphocyte th1 th2

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Control of lymphocyte functions by gut microbiota-derived short-chain fatty acids

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Cellular & Molecular Immunology 2021年第5期18卷 1161-1171页

作者： Chang H.Kim Department of Pathology and Mary H.Weiser Food Allergy Center University of Michigan School of MedicineAnn ArborMIUSA

A mounting body of evidence indicates that dietary fiber(DF)metabolites produced by commensal bacteria play essential roles in balancing the immune system.DF,considered nonessential nutrients in the past,is now considered to be necessary to maintain adequate levels of immunity and suppress inflammatory and allergic responses.Short-chain fatty acids(SCFAs),such as acetate,propionate,and butyrate,are the major DF metabolites and mostly produced by specialized commensal bacteria that are capable of breaking down DF into simpler saccharides and further metabolizing the saccharides into SCFAs.SCFAs act on many cell types to regulate a number of important biological processes,including host metabolism,intestinal functions,and immunity system.this review specifically highlights the regulatory functions of DF and SCFAs in the immune system with a focus on major innate and adaptive lymphocytes.Current information regarding how SCFAs regulate innate lymphoid cells,T helper cells,cytotoxic T cells,and B cells and how these functions impact immunity,inflammation,and allergic responses are discussed.

关键词： Microbiota Dietary fiber Short-chain fatty acids Innate lymphoid cells B cells th1 th17 Tregs CD8 Microbial metabolites

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