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Checkpoint receptor TIGIT mediates NK cell exhaustion

Checkpoint receptor TIGIT mediates NK cell exhaustion

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第十三届全国免疫学学术大会

作者： Jiacheng Bi Qing Zhang Xiaodong Zheng Yongyan Chen Hui Peng Haiming Wei Rui Sun Zhigang Tian University of Science and Technology of China Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences

Checkpoint blockade reverses anti-tumor effector T cell exhaustion,and benefits a subset of patients with a broad spectrum of *** cells are potent anti-tumor effector *** cell frequency has been shown to correlate with patient responsiveness to anti-PD-1 *** showed that absence of NK cells further aggravated exhaustion of tumor-infiltrating CD8T cells,and that therapeutic effects of PD-L1 blockade were dependent on NK cells,highlighting the role of NK cells in tumor ***,NK cells are usually functionally exhausted in tumors,limiting their effector *** underlying mechanisms remained poorly ***,transcriptome analysis of tumor-infiltrating NK cells revealed that Tigit gene was highly expressed in tumor-infiltrating NK *** further showed that TIGIT expression on mouse NK cells was up-regulated not only upon NK cell activation during acute tissue injury and tissue regeneration,but also along NK cell exhaustion in *** functioned to suppress NK cell activity in these contexts,and importantly,to mediate NK cell exhaustion in *** of TIGIT reversed NK cell exhaustion,promoted NK-dependent tumor immunity,and enhanced therapy of PD-L1 blockade when used in *** work demonstrates the critical role of NK cells in checkpoint blockade therapy,and that TIGIT is an important checkpoint on NK *** TIGIT alone or in combination with other checkpoint receptors might be a promising anti-tumor therapeutic strategy.

关键词： inhibitory receptor dysfunction immune evasion antibody

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Heterogeneity of HLA-G expression in cancers:Clinical relevance and potential in therapy

Heterogeneity of HLA-G expression in cancers:Clinical releva...

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浙江省免疫学会第六次会员代表大会暨第十一次学术大会

作者： Wei-Hua Yan Medical Research Center Taizhou Hospital of Zhejiang Province

Phenotypic heterogeneity has been observed in most malignancies,which represents a considerable challenge for tumour *** recent decades,the biological function and clinical significance of the human leukocyte antigen(HLA)-G have been intensively *** is now widely accepted that HLA-G is a critical marker of immunotolerance in cancer cell immune evasion and is strongly associated with disease progress and prognosis for cancer ***,it has recently been emphasized that the signalling pathway linking HLA-G and immunoglobulin-like transcripts(ILTs)is considered an immune *** addition,HLA-G itself can generate at least seven distinct isoforms,and intertumour and intratumour heterogeneity of HLA-G expression is common across different tumour ***,HLA-G heterogeneity in cancers has been related to disease stage and outcomes,metastatic status and response to different *** review focuses on the heterogeneity of HLA-G expression in malignant lesions,and clinical implications of this heterogeneity that might be relevant to personalized treatments are also discussed.

关键词： HLA-G heterogeneity cancer immune evasion therapy target

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Novel immune invasion mechanisms of human important pathogens

Novel immune invasion mechanisms of human important pathogen...

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第十一届全国免疫学学术大会

作者： Zhang Xiao-Lian Wuhan University School of Medicine Dept.of Immunology

Aims: Many human important pathogens cause chronic or latent infections. However their immune invasion mechanisms remain elusive. Methods and results: Mannose-capped lipoarabinomanan(ManLAM) is a lipoglycan serving as a major cell wall component in Mycobacterium tuberculosis(***). Here, we demonstrated a novel ManLAM mediated immune evasion mechanism by inhibitory effects on the polarizations of M1 macrophages and Th1/Th17 cells via CD44. ManLAM induced IL-10 production by upregulating PI3K/AKT signaling pathways in B cells mainly via TLR2, next Mannose receptor(MR). These B10 cells skew CD8 T towards a Th2 subtype. We also found that novel viral immune invasion mechanisms mediated by the specific N-glycans and G-quadruplex of Hepatitis C Virus(HCV).Conclusions: Collectively, these fndings provide a novel mechanism in which *** ManLAM negatively regulates host anti-TB immunity and Man LAM is potential as a novel therapeutic agent in autoimmunity. Our data demonstrate that an aptamer specifically against ManLAM with low and no toxicity, holds a potential antimycobacterial agent and tuberculosis vaccine immune ***(Zhang X-L*, et al, JACS, 2016;Zhang X-L*, et al, Mol Therapy, 2014;Zhang X.L. et al, J Infect. 2016, 2015, 2014). Our data also provide new G-quadruplex/N-glycan-targeting anti-HCV strategy(Zhang X.L*, et al, Science Advances, 2016;Zhang X.-L*, et al, J Immunol, 2014;Zhang X.-L*. et al.,BBA, 2016).

关键词： immune evasion Mycobacterium tuberculosis HCV ManLAM N-glycosylation G-quadruplex

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Identification and characterization of a novel Plasmodium vivax exported protein PvEXP100

Identification and characterization of a novel Plasmodium vi...

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第十一届全国寄生虫学青年工作者学术研讨会

作者： Xinxin Zhang Ruilin Chu Haitian Fu Xiaodan Shi Yinghua Xuan Yang Cheng Laboratory of Pathogen Infection and Immunity Department of Public Health and Preventive MedicineWuxi School of MedicineJiangnan University

Malaria is one of the serious infectious diseases of humans in the world,and vivax malaria is the most geographically widespread of the human *** is widely accepted that during parasite invasion and development within host cells,*** exported protein specifically cytoadhere to human spleen fibroblast(HSF) cells where they are protected from macrophage clearance and upon disruption of barrier cells during crisis,free merozoites will immediately ***,the detailed mechanism is still *** investigated a hypothetic *** protein Pv EXP100 in blood *** assay data reveals that Pv EXP100 is a novel protein which exported to infected red blood cell surface,and anti-Pv EXP100 causes partial immune response(sensitivity 42%,specificity 96.9%).Additionally,the data showed Pv EXP100 drove HSF cells migration,and Pv EXP100 could bind HSF *** summary,Pv EXP100 is a novel exported protein that may be a potential molecule involved in the immune evasion of ***.

关键词： Plasmodium vivax export protein human spleen fibroblast immune evasion

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Trichinella spiralis calreticulin inhibits the complement classical pathway activation by interaction with human complement C1q

Trichinella spiralis calreticulin inhibits the complement cl...

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中国动物学会寄生虫学专业委员会第十届全国寄生虫学青年工作者学术研讨会

作者： Limei Zhao Shuai Shao Yi Chen Jing Yang Xinping Zhu Department of Parasitology School of Basic Medical Sciences Capital Medical University

Objective To explore the role of Trichinella spiralis calreticulin(Ts-CRT) in host immune attack by interference with the complement function, therefore deeply clarifying the mechanisms of *** evading from complement killing Methods Recombinant Ts-CRT(r Ts-CRT) was expressed and its ability to bind calcium was assessed using "Stains-all". The expression pattern and distribution of Ts-CRT were detected by Western blot and confocal immunofluorescence. The binding between r Ts-CRT and C1 q was determined by ELISA, Far Western blot and co-immunoprecipitation. The activation products of C4/C3 deposition were detected with ELISA and the complement-mediated lysis of sheep erythrocytes was investigated with hemolysis assay. The effect of r Ts-CRT on C1 q interacting with its receptor on THP-1-derived macrophages was examined by cell immunofluorescence staining and the C1q-induced chemotaxis of macrophages was determined by Transwell. Results The results of "Stains-all" suggested that r Ts-CRT had the ability to bind Ca2+. ELIAS and expressed all the developmental stages. Far Western blot and co-immunoprecipitation experiments showed that r Ts-CRT was able to bind human C1 q. The interaction of rT s-CRT and C1 q significantly reduced C4 and C3 deposition to the activator Ig M. The C1q-dependent lysis of sensitized sheep erythrocytes was also inhibited by r Ts-CRT. rT s-CRT also inhibited C1 q interacting with its receptor on THP-1-derived M2 phenotype macrophage and suppressed C1q-induced macrophages chemotaxis. Conclusion These findings suggest that Ts-CRT plays an important role in the immune evasion by inhibiting the initial stage of host complement activation.

关键词： Trichinella spiralis calrecitulin complement C1q immune evasion complement attack

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The IFN-γ/PD-L1 axis between T cells and tumor microenvironment: hints for glioma anti-PD-1/PD-L1 therapy

The IFN-γ/PD-L1 axis between T cells and tumor microenviron...

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第十三届全国免疫学学术大会

作者： Jiawen Qian Chen Wang Bo Wang Yiwei Chu Department of Basic Medicine Shanghai Medical CollegeFudan University

Backgound: PD-L1 is an immune inhibitory receptor ligand that leads to T cell dysfunction and apoptosis by binding to its receptor PD-1, which works in braking inflammatory response and conspiring tumor immune evasion. However, in gliomas, the cause of PD-L1 expression in tumor microenvironment is not yet clear. Besides, auxiliary biomarkers are urgently needed for screening possible responsive glioma patients for anti-PD-1/PD-L1 ***: The distribution of tumor infiltrating T cells and PD-L1 expression was analyzed via immunofluorescence in orthotopic murine glioma model. The expression of PD-L1 in immune cell populations was detected by flow cytometry. Data excavated from TCGA LGG/GBM datasets and the Ivy Glioblastoma Atlas Project was used for in silico analysis of the correlation among genes and ***: The distribution of tumor infiltrating T cells and PD-L1 expression, which parallels in murine orthotopic glioma model and human glioma microdissections, was interrelated. The IFN-γ level was positively correlated with PD-L1 expression in murine glioma. Further, IFN-γ induces PD-L1 expression on primary cultured microglia, BMDM and GL261 glioma cells in vitro. Seven IFN-γ induced genes, namely GBP5, ICAM1, CAMK2 D, IRF1, SOCS3, CD44 and CCL2, were selected to calculate IFN-γ score as substitute indicator for IFN-γ level. IFN-γ score were positively correlated with PD-L1 expression in different anatomic structures of human glioma and in glioma of staged ***: Our study identified the distribution of tumor infiltrating T cells and PD-L1 expression in murine glioma model and human glioma samples. And we found that IFN-γ is an important cause of PD-L1 expression in glioma microenvironment. Further, we proposed IFN-γ score aggregated from the expressions of the listed IFN-γ induced genes as a complementary prognostic indicator for anti-PD-1/PD-L1 therapy.

关键词： PD-L1 IFN-γ glioma immune evasion

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The Pathway of Myeloid-Derived Suppressor Cells on T cells during Japanese Encephalitis Virus Infection

The Pathway of Myeloid-Derived Suppressor Cells on T cells d...

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第十三届全国免疫学学术大会

作者： Xiaochen Gao Nan Zhang Min Cui Huazhong Agricultural University

Japanese encephalitis virus(JEV) can invade into the central nervous system(CNS) leading to severe neuroinflammation even death, however, the mechanism of JEV evasion from the immune system is not *** this study, the 6-8 week old female C57BL/6 mice were infected with virulent strain of JEV P3 intravenously(i.v.).On 1-5 days post infection(d.p.i), splenocytes were collected every other day for the detection of myeloid-derived suppressor cells(MDSCs) and T cells by flow *** was found that the number of CD11bGr-1 cells(MDSCs) increased and CD3CD4 T cells gradually decreased accordingly at the same time of P3 *** ELISA showed that Arg-1 and NO were increased with the P3 *** expression of CD62L on CD4 T cells decreased along with the upregulation of ADAM17 on *** further study the pathway of P3-induced MDSCs affected on CD4 T cells, P3-induced MDSCs were sorted and cocultured with CD4 T cells.P3-induced MDSCs significantly suppressed CD4 T cells proliferation with stimulation of ***, with the treatment of inhibitor TAPI-1, 1400 W, or NAC in the co-culture system, the effects of MDSCs on CD4 T cells was suppressed, especially with iNOS inhibitor 1400 *** findings indicate that MDSCs mediated P3 evasion from the immune responses potentially via the iNOS pathway.

关键词： JEV MDSCs immune evasion iNOS

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N4-Acetylcytidine of FOXP1 promotes cervical cancer progression via driving metabolic reprogramming

N4-Acetylcytidine of FOXP1 promotes cervical cancer progress...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Xiaona Chen Shenzhen Hospital Southern Medical University 南方医科大学第三临床学院

Objective: Mounting evidences showed that metabolic reprogramming and immune evasion, known as the hallmarks of cancer, are the main causes of the progression and prognosis in cervical squamous cell carcinoma(CSCC). However, little is known about the interaction between the tumor metabolism remodeling and tumor microenvironment(TME) in CSCC. Futhermore, N4-acetylcytidine(ac4 C),which has been considered as an epitranscriptomic RNA modification on human mRNA,involved in mRNA transcriptional translation process, plays a vital role in the development,progression, and prognosis of cancer. In this study, we identified that N4-Acetylcytidine(ac4 C) RNA acetylation of FOXP1 catalyzed by acetyltransferase NAT10 is closely related to the progression of cervical squamous cell carcinoma, which instigates immunosuppression by utilizing the increased glycolysis of cancer cells, to futher explore immunotherapeutic potential of targeting cancer metabolism in ***: Immunohistochemistry and tissue microarray were used to evaluate the expression of NAT10 and FOXP1 in CSCC tissues. The effects of NAT10 on the development of CSCC were investigated through in vitro and in vivo assays. Moreover, the ac4 C of FOXP1 catalyzed by NAT10 in CSCC cells was quantified through acRIP-sequencing as well as ac4 C acetylated RNA immunoprecipitation quantitative reverse transcription polymerase chain reaction(acRIP qRTPCR)assay. Futher, glycolytic activity was identificated by the extracellular acidification rate kinetic profiles using seahorse *** investigate the mechanism of immune evasion caused by tumor microenvironment, we examined the tumor-infiltrating immune cells in murine models through Flow ***: Here, we interrogated that the level of ac4 C RNA was significantly increased in CSCC, and NAT10 expression, a regulator involved in the abundant ac4 C RNA modification, was significantly elevated in CSCC tissues with development of tumor and associated with tumor metastas

关键词： Cervical squamous cell carcinoma ac4C modification NAT10-ac4c-FOXP1 axis metabolic reprogramming immune evasion

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N4-Acetylcytidine of FOXP1 promotes cervical squamous cell carcinoma progression via driving metabolic reprogramming

N4-Acetylcytidine of FOXP1 promotes cervical squamous cell c...

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2021年中国肿瘤标志物学术大会暨第十五届肿瘤标志物青年科学家论坛

作者： Xiaona Chen Sheng Zhong Xia Guo

Objective: Mounting evidences showed that metabolic reprogramming and immune evasion, known as the hallmarks of cancer, are the main causes of the progression and prognosis in cervical squamous cell carcinoma(CSCC). However, little is known about the interaction between the tumor metabolism remodeling and tumor microenvironment(TME) in CSCC. Furthermore, N4-acetylcytidine(ac4 C),which has been considered as an epitranscriptomic RNA modification on human mRNA, involved in mRNA transcriptional translation process, plays a vital role in the development, progression, and prognosis of cancer. In this study, we identified that N4-Acetylcytidine(ac4 C) RNA acetylation of FOXP1 catalyzed by acetyltransferase NAT10 is closely related to the progression of cervical squamous cell carcinoma, which instigates immunosuppression by utilizing the increased glycolysis of cancer cells, to further explore immunotherapeutic potential of targeting cancer metabolism in ***: Immunohistochemistry and tissue microarray were used to evaluate the expression of NAT10 and FOXP1 in CSCC tissues. The effects of NAT10 on the development of CSCC were investigated through in vitro and in vivo assays. Moreover, the ac4 C of FOXP1 catalyzed by NAT10 in CSCC cells was quantified through acRIP-sequencing as well as ac4 C acetylated RNA immunoprecipitation quantitative reverse transcription polymerase chain reaction(acRIP qRT-PCR) assay. Further,glycolytic activity was identificated by the extracellular acidification rate kinetic profiles using seahorse XF96. To investigate the mechanism of immune evasion caused by tumor microenvironment,we examined the tumor-infiltrating immune cells in murine models through Flow ***: Here, we interrogated that the level of ac4 C RNA was significantly increased in CSCC, and NAT10 expression, a regulator involved in the abundant ac4 C RNA modification, was significantly elevated in CSCC tissues with development of tumor and associated with tumor me

关键词： Cervical squamous cell carcinoma ac4c modification NAT10-ac4c-FOXP1 axis metabolic reprogramming immune evasion

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Vif from HIV Inhibits Inflammation in Macrophages through ITIMs

Vif from HIV Inhibits Inflammation in Macrophages through IT...

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第十二届全国免疫学学术大会

作者：严大鹏王于复旦大学

immune evasion is a common strategy for the successful infection of the host by *** the importance of protein Vif in HIV-1 replication,relatively little is known about the role of Vif in the regulation of host innate ... 详细信息

关键词： Vif HIV ITIMs immune evasion

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