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Continuous Expression of Interferon Regulatory Factor 4 Sustains CD8^(+)T Cell Immunity against Tumor

Research 2024年第3期2023卷 433-444页

作者： Anze Yu Jinfei Fu Zheng Yin Hui Yan Xiang Xiao Dawei Zou Xiaolong Zhang Xiongbing Zu Xian C.Li Wenhao Chen Immunobiology and Transplant Science Center Department of SurgeryHouston Methodist Research Institute and Institute for Academic MedicineHouston Methodist HospitalHoustonTXUSA Department of Urology First Affiliated HospitalSun Yat-sen UniversityGuangzhouGuangdongChina Systems Medicine and Bioengineering Department Houston Methodist Neal Cancer CenterHoustonTXUSA Department of Radiology Houston Methodist HospitalWeill Cornell MedicineHoustonTXUSA Department of Urology Xiangya HospitalCentral South UniversityChangshaHunanChina Department of Surgery Weill Cornell MedicineCornell UniversityNew YorkNYUSA.

T-cell-based immunotherapy is gaining momentum in cancer treatment;however,our comprehension of the transcriptional regulation governing T cell antitumor activity remains *** objective of this study was to explore the function of interferon regulatory factor 4(IRF4)in antitumor CD8^(+)T cells using the TRAMP-C1 prostate cancer and B16F10 melanoma *** achieve this,we generated an Irf4^(GFP-DTR) mouse strain and discovered that CD8^(+)tumor-infiltrating lymphocytes(TILs)expressing high levels of *** exhibited a more differentiated PD-1high cell *** administering diphtheria toxin to tumor-bearing Irf4^(GFP-DTR) mice,we partially depleted ***^(+)TILs and observed an accelerated tumor *** specifically explore the function of IRF4 in antitumor CD8^(+)T cells,we conducted 3 adoptive cell therapy(ACT)***,depleting ***^(+)CD8^(+)TILs derived from ACT significantly accelerated tumor growth,emphasizing their crucial role in controlling tumor ***,deleting the Irf4 gene in antitumor CD8^(+)T cells used for ACT led to a reduction in the frequency and effector differentiation of CD8^(+)TILs,completely abolishing the antitumor effects of ***,we performed a temporal deletion of the Irf4 gene in antitumor CD8^(+)T cells during ACT,starting from 20 days after tumor implantation,which significantly compromised tumor ***,sustained expression of IRF4 is essential for maintaining CD8^(+)T cell immunity in the melanoma model,and these findings carry noteworthy implications for the advancement of more potent immunotherapies for solid tumors.

关键词： sustained immunity implantation

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CD300ld: A new target for tumor immunotherapy and new hope for cancer patients

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Science Bulletin 2024年第17期69卷 2653-2655页

作者： Huiqin Chen Guanqun Guo Gen Yang Wenzhou institute University of Chinese Academy of SciencesWenzhou 325000China School of Physics Peking UniversityBeijing 100871China

In recent years, immune checkpoint blockade (ICB) therapy,represented by molecules such as programmed cell death 1 (PD-1), programmed death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), has made revolutionary progress in the field of tumor treatment. However, the efficacy of ICB in different clinical cancer patients varies greatly, with most patients showing little or no response to the treatments [1]. The suppressive tumor immune microenvironment (TME) containing high myeloid cells is a major cause of the failure of immunotherapy[2,3].

关键词： patients immunotherapy CD30

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MicroRNA in vivo precipitation identifies miR-151-3p as a computational unpredictable miRNA to target Stat3 and inhibits innate IL-6 production

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Cellular & Molecular Immunology 2018年第2期15卷 99-110页

作者： Xiang Liu Xiaoping Su Sheng Xu Huamin Wang Dan Han Jiangxue Li Mingyan Huang Xuetao Cao National Key Laboratory of Medical Immunology&institute of Immunology Second Military Medical UniversityShanghai200433China Department of Immunology&Center for immunotherapy Institute of Basic Medical SciencesPeking Union Medical CollegeChinese Academy of Medical SciencesBeijing100005China institute of Immunology Zhejiang University School of MedicineHangzhou310058China

MicroRNAs(miRNAs)function as important regulators in the immune response and *** approaches have been reported to computationally predict miRNAs and their potential ***,there are still many miRNA–target interactions that are unpredictable by using the current computational *** established a miRNA in vivo precipitation method(miRIP)to identify unpredictable miRNAs with definite targets in these *** Stat3 is a well-known transcription factor involved in innate immunity and inflammation,we utilized the miRIP method to identify miRNAs that bind Stat3 mRNA in *** the captured miRNAs,miR-151-3p was confirmed to interact with Stat3 mRNA 3′-UTR and downregulate the Stat3 protein *** stimulation decreased miR-151-3p expression,thereby increasing IL-6 ***,we found that miR-151-3p inhibited LPS-induced IL-6 production by targeting *** data further confirmed miRIP as an efficient method to identify unpredictable miRNAs and explore miRNAs-mediated regulation in innate immunity and inflammation.

关键词： innate immunity IL-6 macrophage miR-151-3p Stat3

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Methyltransferase Dot1l preferentially promotes innate IL-6 and IFN-β production by mediating H3K79me2/3 methylation in macrophages

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Cellular & Molecular Immunology 2020年第1期17卷 76-84页

作者： Xiang Chen Xingguang Liu Yunkai Zhang Wanwan Huai Qingqing Zhou Sheng Xu Xi Chen Nan Li Xuetao Cao National Key Laboratory of Medical Immunology&institute of Immunology Second Military Medical UniversityShanghai 200433China institute of Immunology Zhejiang University School of MedicineHangzhou 310058China Department of Immunology&Center for immunotherapy Institute of Basic Medical SciencesPeking Union Medical CollegeChinese Academy of Medical SciencesBeijing 100005China

Epigenetic modification,including histone modification,precisely controls target gene *** posttranscriptional regulation of the innate signaling-triggered production of inflammatory cytokines and type I interferons has been fully elucidated,whereas the roles of histone modification alteration and epigenetic modifiers in regulating inflammatory responses need to be further ***/tri-methylation modifications of histone 3 lysine 79(H3K79me2/3)have been shown to be associated with gene transcriptional *** of telomeric silencing-1-like(Dot1l)is the only known exclusive H3K79 methyltransferase and regulates the proliferation and differentiation of tumor ***,the roles of Dot1l and Dot1l-mediated H3K79 methylation in innate immunity and inflammatory responses remain ***,we found that H3K79me2/3 modification levels at the Il6 and Ifnb1 promoters,as well as H3K79me2 modification at the Tnfαpromoter,were increased in macrophages activated by Toll-like receptor(TLR)ligands or virus *** innate signals upregulated Dot1l expression in macrophages and THP1 ***1l silencing or a Dot1l inhibitor preferentially suppressed the production of IL-6 and interferon(IFN)-βbut not of TNFαin macrophages and THP1 cells triggered by TLR ligands or virus ***1l was recruited to the proximal promoter of the Il6 and Ifnb1 but not Tnfαgene and then mediated H3K79me2/3 modification at the Il6 and Ifnb1 promoters,consequently facilitating the transcription and expression of Il6 and ***,Dot1l-mediated selective H3K79me2/3 modifications at the Il6 and Ifnb1 promoters are required for the full activation of innate immune *** finding adds new insights into the epigenetic regulation of inflammatory responses and pathogenesis of autoimmune diseases.

关键词： H3K79me2/3 Dot1l epigenetic regulation IL-6 IFN-β macrophages inflammation

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Development of a potent benzonitrile-based inhibitor of glutaminyl-peptide cyclotransferase-like protein(QPCTL)with antitumor efficacy

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Signal Transduction and Targeted Therapy 2024年第1期9卷 44-46页

作者： Lei Yu Pengcheng Zhao Yaoliang Sun Zening Zheng Wenhao Du Lishan Zhang Yaxu Li Longyan Xie Shilin Xu Ping Wang Tongji University Cancer Center Shanghai Tenth People’s HospitalSchool of MedicineTongji UniversityShanghaiChina Department of Medicinal Chemistry Shanghai Institute of Materia MedicaChinese Academy of SciencesShanghaiChina

Dear Editor,Immune checkpoint therapies manipulating the immune system to eliminate tumor cells have shown remarkable clinical efficacy in treating various ***47,an emerging efficient immune checkpoint,is crucial for cancer cells to evade macrophagemediated phagocytosis by interaction with signal-regulatory proteinα(SIRPα).Antibodies blocking the CD47/SIRPαinteraction have been effective to promote macrophage-mediated phagocytosis in various types of cancer in mice and ***47 is not only highly expressed in tumor cells,but also normal cells,such as red blood cells(RBCs).Thus,during clinical trials involving cancer patients,anti-CD47 antibodies may promote the macrophagesmediated phagocytosis of RBCs,ultimately inducing undesirable anemia side *** contrast,small molecule inhibitors interrupting CD47/SIRPαaxis have shown potential to overcome the anemia,possibly due to their lower immunogenicity and shorter half-life compared to antibodies.1 Hence,developing the novel strategies,especially those without the anemia side effect,to intervene in CD47/SIRPαinteraction will benefit cancer immunotherapy.

关键词： anemia overcome eliminate

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T cell receptor signaling and cell immunotherapy

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National Science Open 2024年第4期3卷 156-171页

作者： Linsong Zhang Xinyi Xu Xiaoshan Shi Chenqi Xu Key Laboratory of Quantitative Synthetic Biology Shenzhen Institute of Synthetic Biology Shenzhen Institute of Advanced TechnologyChinese Academy of Sciences State Key Laboratory of Molecular Biology CAS Center for Excellence in Molecular Cell Science Shanghai Institute of Biochemistry and Cell Biology University of Chinese Academy of Sciences Chinese Academy of Sciences

As the major sensor of adaptive immune system, T cell receptor(TCR) can recognize diverse antigens and initiate specific immune responses against invading pathogens and cancer cells. Understanding the mechanisms of TCR signaling has led to the development of engineered T cell therapies, which have extensive applications in the treatment of diseases such as cancer, infection and autoimmunity. Here, we review the current understanding of antigen-induced TCR signaling and discuss its applications in T cell therapies.

关键词： T cell receptor-CD3 complex signaling T cell therapy

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Deep learning framework for comprehensive molecular and prognostic stratifications of triple-negative breast cancer

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Fundamental Research 2024年第3期4卷 678-689页

作者： Shen Zhao Chao-Yang Yan Hong Lv Jing-Cheng Yang Chao You Zi-Ang Li Ding Ma Yi Xiao Jia Hu Wen-Tao Yang Yi-Zhou Jiang Jun Xu Zhi-Ming Shao Key Laboratory of Breast Cancer in Shanghai Department of Breast SurgeryFudan University Shanghai Cancer CenterShanghai 200032China institute for AI in Medicine School of Artificial IntelligenceNanjing University of Information Science and TechnologyNanjing 210044China Department of Pathology Fudan University Shanghai Cancer CenterShanghai 200032China Greater Bay Area institute of Precision Medicine Guangzhou 511466China Department of Radiology Fudan University Shanghai Cancer CenterShanghai 200032China

Triple-negative breast cancer(TNBC)is the most challenging breast cancer *** stratification and target therapy bring clinical benefit for TNBC patients,but it is difficult to implement comprehensive molecular testing in clinical ***,using our multi-omics TNBC cohort(N=425),a deep learning-based framework was devised and validated for comprehensive predictions of molecular features,subtypes and prognosis from pathological whole slide *** framework first incorporated a neural network to decompose the tissue on WSIs,followed by a second one which was trained based on certain tissue types for predicting different ***-omics molecular features were analyzed including somatic mutations,copy number alterations,germline mutations,biological pathway activities,metabolomics features and immunotherapy *** was shown that the molecular features with therapeutic implications can be predicted including the somatic PIK3CA mutation,germline BRCA2 mutation and PD-L1 protein expression(area under the curve[AUC]:0.78,0.79 and 0.74 respectively).The molecular subtypes of TNBC can be identified(AUC:0.84,0.85,0.93 and 0.73 for the basal-like immune-suppressed,immunomodulatory,luminal androgen receptor,and mesenchymal-like subtypes respectively)and their distinctive morphological patterns were revealed,which provided novel insights into the heterogeneity of TNBC.A neural network integrating image features and clinical covariates stratified patients into groups with different survival outcomes(log-rank P<0.001).Our prediction framework and neural network models were externally validated on the TNBC cases from TCGA(N=143)and appeared robust to the changes in patient *** potential clinical translation,we built a novel online platform,where we modularized and deployed our framework along with the validated *** can realize real-time one-stop prediction for new *** summary,using only pathological WSIs,our proposed framework

关键词： Triple-negative breast cancer Deep learning Digital pathology Patient stratification Online platform

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Cellular and molecular regulation of innate inflammatory responses

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Cellular & Molecular Immunology 2016年第6期13卷 711-721页

作者： Juan Liu Xuetao Cao National Key Laboratory of Medical Immunology & institute of Immunology Second Military Medical University Shanghai 200433 China National Key Laboratory of Medical Molecular Biology Department of Immunology & Center for Immunotherapy Institute of Basic Medical Sciences Peking Union Medical College Chinese Academy of Medical Sciences Beijing 100005 China

Innate sensing of pathogens by pattern-recognition receptors （PRRs） plays essential roles in the innate discrimination between self and non-self components, leading to the generation of innate immune defense and inflammatory responses. The initiation, activation and resolution of innate inflammatory response are mediated by a complex network of interactions among the numerous cellular and molecular components of immune and non- immune system. While a controlled and beneficial innate inflammatory response is critical for the elimination of pathogens and maintenance of tissue homeostasis, dysregulated or sustained inflammation leads to pathological conditions such as chronic infection, inflammatory autoimmune diseases. In this review, we discuss some of the recent advances in our understanding of the cellular and molecular mechanisms for the establishment and reJzulation of innate immunity and inflammatory responses.

关键词： dendritic cells inflammation innate lymphoid cells innate signaling pattern-recognition receptors (PRRs)

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The function and regulation of TET2 in innate immunity and inflammation

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Protein & Cell 2021年第3期12卷 165-173页

作者： Boyi Cong Qian Zhang Xuetao Cao Laboratory of Immunity and Inflammation College of Life SciencesNankai UniversityTianjin 300071China National Key Laboratory of Medical Immunology Institute of ImmunologyNavy Military Medical UniversityShanghai 200433China Department of Immunology Center for ImmunotherapyInstitute of Basic Medical SciencesChinese Academy of Medical SciencesBeijing 100005China

TET2,a member of ten-eleven translocation(TET)family as a-ketoglutarate-and Fe2+-dependent dioxygenase catalyzing the iterative oxidation of 5-methylcytosine(5mC),has been widely recognized to be an important regulator for normal hematopoiesis especially *** and dysregulation of TET2 contribute to the development of multiple hematological *** studies reveal that TET2 also plays an important role in innate immune homeostasis by promoting DNA demethylation or independent of its enzymatic ***,we focus on the functions of TET2 in the initiation and resolution of inflammation through epigenetic regulation and signaling *** addition,we highlight regulation of TET2 at various molecular levels as well as the correlated inflammatory diseases,which will provide the insight to intervene in the pathological process caused by TET2 dysregulation.

关键词： TET2 innate immune response DNA demethylation inflammatory resolution inflammatory diseases

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Targeting carnitine palmitoyl transferase 1A(CPT1A)induces ferroptosis and synergizes with immunotherapy in lung cancer

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Signal Transduction and Targeted Therapy 2024年第4期9卷 1675-1689页

作者： Lei Ma Chong Chen Chunxing Zhao Tong Li Lingyu Ma Jiayu Jiang Zhaojun Duan Qin Si Tsung-Hsien Chuang Rong Xiang Yunping Luo Department of Immunology Institute of Basic Medical SciencesChinese Academy of Medical SciencesSchool of Basic MedicinePeking Union Medical CollegeBeijing 100005China Collaborative Innovation Center for Biotherapy Institute of Basic Medical SciencesChinese Academy of Medical SciencesSchool of Basic MedicinePeking Union Medical CollegeBeijing 100005China Department of Lung Cancer Surgery Tianjin Medical University General HospitalTianjin 300052China Immunology Research Center National Health Research InstitutesZhunanMiaoliTaiwanROC Department of Immunology Nankai UniversityTianjin 300071China

Despite the successful application of immune checkpoint therapy,no response or recurrence is typical in lung *** stem cells(CSCs)have been identified as a crucial player in immunotherapy-related ***,a form of cell death driven by iron-dependent lipid peroxidation,is highly regulated by cellular metabolism remolding and has been shown to have synergistic effects when combined with *** adaption of CsCs drives tumor resistance,yet the mechanisms of their ferroptosis defense in tumor immune evasion remain ***,through metabolomics,transcriptomics,a lung epithelialspecific Cptla-knockout mouse model,and clinical analysis,we demonstrate that CPT1A,a key rate-limiting enzyme of fatty acid oxidation,acts with L-carnitine,derived from tumor-associated macrophages to drive ferroptosis-resistance and CD8^(+)T cells inactivation in lung ***,CPT1A restrains ubiquitination and degradation of c-Myc,while c-Myc transcriptionally activates CPT1A *** CPT1A/c-Myc positive feedback loop further enhances the cellular antioxidant capacity by activating the NRF2/GPX4 system and reduces the amount of phospholipid polyunsaturated fatty acids through ACSL4 downregulating,thereby suppressing ferroptosis in ***,targeting CPT1A enhances immune checkpoint blockadeinduced anti-tumor immunity and tumoral ferroptosis in tumor-bearing *** results illustrate the potential of a mechanismguided therapeutic strategy by targeting a metabolic vulnerability in the ferroptosis of CsCs to improve the efficacy of lung cancer immunotherapy.

关键词： immunotherapy metabolism peroxidation

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