Science Immunology最新文献_第10页

CAR-ving away OX40L with engineered Tregs 利用工程化 Tregs 清除 OX40L。

IF 17.6 1区医学

Science Immunology Pub Date : 2024-11-01 DOI: 10.1126/sciimmunol.adu0983

Jonathan S. Maltzman

引用次数: 0

The pore-forming apolipoprotein APOL7C drives phagosomal rupture and antigen cross-presentation by dendritic cells 形成孔隙的载脂蛋白 APOL7C 驱动吞噬体破裂和树突状细胞的抗原交叉呈递

IF 17.6 1区医学

Science Immunology Pub Date : 2024-11-01 DOI: 10.1126/sciimmunol.adn2168

Gerone A. Gonzales, Song Huang, Liam Wilkinson, Jenny A. Nguyen, Saif Sikdar, Cécile Piot, Victor Naumenko, Jahanara Rajwani, Cassandra M. Wood, Irene Dinh, Melanie Moore, Eymi Cedeño, Neil McKenna, Maria J. Polyak, Sara Amidian, Vincent Ebacher, Nicole L. Rosin, Matheus B. Carneiro, Bas Surewaard, Nathan C. Peters, Christopher H. Mody, Jeff Biernaskie, Robin M. Yates, Douglas J. Mahoney, Johnathan Canton

{"title":"The pore-forming apolipoprotein APOL7C drives phagosomal rupture and antigen cross-presentation by dendritic cells","authors":"Gerone A. Gonzales, Song Huang, Liam Wilkinson, Jenny A. Nguyen, Saif Sikdar, Cécile Piot, Victor Naumenko, Jahanara Rajwani, Cassandra M. Wood, Irene Dinh, Melanie Moore, Eymi Cedeño, Neil McKenna, Maria J. Polyak, Sara Amidian, Vincent Ebacher, Nicole L. Rosin, Matheus B. Carneiro, Bas Surewaard, Nathan C. Peters, Christopher H. Mody, Jeff Biernaskie, Robin M. Yates, Douglas J. Mahoney, Johnathan Canton","doi":"10.1126/sciimmunol.adn2168","DOIUrl":"10.1126/sciimmunol.adn2168","url":null,"abstract":"<div >Conventional dendritic cells (cDCs) generate protective cytotoxic T lymphocyte (CTL) responses against extracellular pathogens and tumors. This is achieved through a process known as cross-presentation (XP), and, despite its biological importance, the mechanism(s) driving XP remains unclear. Here, we show that a cDC-specific pore-forming protein called apolipoprotein L 7C (APOL7C) is up-regulated in response to innate immune stimuli and is recruited to phagosomes. Association of APOL7C with phagosomes led to phagosomal rupture and escape of engulfed antigens to the cytosol, where they could be processed via the endogenous MHC class I antigen processing pathway. Accordingly, mice deficient in APOL7C did not efficiently prime CD8<sup>+</sup> T cells in response to immunization with bead-bound and cell-associated antigens. Together, our data indicate the presence of dedicated apolipoproteins that mediate the delivery of phagocytosed proteins to the cytosol of activated cDCs to facilitate XP.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 101","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TAM-ing the beast with IL-34 blockade 用 IL-34 阻断 TAM--野兽

IF 17.6 1区医学

Science Immunology Pub Date : 2024-11-01 DOI: 10.1126/sciimmunol.adu0981

Aron Gyorgypal, Robert M. Anthony

引用次数: 0

Orientation-dependent CD45 inhibition with viral and engineered ligands 利用病毒配体和工程配体抑制定向依赖性 CD45

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-25 DOI: 10.1126/sciimmunol.adp0707

Marta T. Borowska, Liu D. Liu, Nathanael A. Caveney, Kevin M. Jude, Won-Ju Kim, Takeya Masubuchi, Enfu Hui, Robbie G. Majzner, K. Christopher Garcia

引用次数: 0

Gastrointestinal germinal center B cell depletion and reduction in IgA+ plasma cells in HIV-1 infection 胃肠道生殖中心 B 细胞耗竭和 HIV-1 感染者 IgA + 浆细胞减少

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-25 DOI: 10.1126/sciimmunol.ado0090

Francesca Cossarini, Joan Shang, Azra Krek, Zainab Al-Taie, Ruixue Hou, Pablo Canales-Herrerias, Minami Tokuyama, Michael Tankelevich, Adam Tillowitz, Divya Jha, Alexandra E. Livanos, Louise Leyre, Mathieu Uzzan, Gustavo Martinez-Delgado, Matthew D. Taylor, Keshav Sharma, Arno R. Bourgonje, Michael Cruz, Giorgio Ioannou, Travis Dawson, Darwin D''Souza, Seunghee Kim-Schulze, Ahmed Akm, Judith A. Aberg, Benjamin K. Chen, Douglas S. Kwon, Sacha Gnjatic, Alexandros D. Polydorides, Andrea Cerutti, Carmen Argmann, Ivan Vujkovic-Cvijin, Mayte Suarez-Fariñas, Francesca Petralia, Jeremiah J. Faith, Saurabh Mehandru

{"title":"Gastrointestinal germinal center B cell depletion and reduction in IgA+ plasma cells in HIV-1 infection","authors":"Francesca Cossarini, Joan Shang, Azra Krek, Zainab Al-Taie, Ruixue Hou, Pablo Canales-Herrerias, Minami Tokuyama, Michael Tankelevich, Adam Tillowitz, Divya Jha, Alexandra E. Livanos, Louise Leyre, Mathieu Uzzan, Gustavo Martinez-Delgado, Matthew D. Taylor, Keshav Sharma, Arno R. Bourgonje, Michael Cruz, Giorgio Ioannou, Travis Dawson, Darwin D''Souza, Seunghee Kim-Schulze, Ahmed Akm, Judith A. Aberg, Benjamin K. Chen, Douglas S. Kwon, Sacha Gnjatic, Alexandros D. Polydorides, Andrea Cerutti, Carmen Argmann, Ivan Vujkovic-Cvijin, Mayte Suarez-Fariñas, Francesca Petralia, Jeremiah J. Faith, Saurabh Mehandru","doi":"10.1126/sciimmunol.ado0090","DOIUrl":"10.1126/sciimmunol.ado0090","url":null,"abstract":"<div >Gastrointestinal (GI) B cells and plasma cells (PCs) are critical to mucosal homeostasis and the host response to HIV-1 infection. Here, high-resolution mapping of human B cells and PCs sampled from the colon and ileum during both viremic and suppressed HIV-1 infection identified a reduction in germinal center (GC) B cells and follicular dendritic cells (FDCs) during HIV-1 viremia. Immunoglobulin A–positive (IgA<sup>+</sup>) PCs are the major cellular output of intestinal GCs and were significantly reduced during viremic HIV-1 infection. PC-associated transcriptional perturbations, including type I interferon signaling, persisted in antiretroviral therapy (ART)–treated individuals, suggesting ongoing disruption of the intestinal immune milieu during ART. GI humoral immune perturbations were associated with changes in the intestinal microbiome composition and systemic inflammation. These findings highlight a key immune defect in the GI mucosa due to HIV-1 viremia.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 100","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ado0090","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142489635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum for the Research Article “Initiator cell death event induced by SARS-CoV-2 in the human airway epithelium” by K. Liang et al. 对 K. Liang 等人的研究文章 "SARS-CoV-2 在人气道上皮细胞中诱导的启动子细胞死亡事件 "的勘误

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-18 DOI: 10.1126/sciimmunol.adt4547

引用次数: 0

Erratum for the Research Article “Circulating KLRG1+ long-lived effector memory T cells retain the flexibility to become tissue resident” by E. D. Lucas et al. E. D. Lucas 等人的研究文章 "循环中的 KLRG1+ 长效记忆 T 细胞具有成为组织常驻细胞的灵活性 "的勘误。

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-18 DOI: 10.1126/sciimmunol.adt4549

引用次数: 0

Programmable bacteria synergize with PD-1 blockade to overcome cancer cell–intrinsic immune resistance mechanisms 可编程细菌与 PD-1 阻断剂协同作用，克服癌细胞内在的免疫抵抗机制

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-18 DOI: 10.1126/sciimmunol.adn9879

Fangda Li, Zaofeng Yang, Thomas M. Savage, Rosa L. Vincent, Kenia de los Santos-Alexis, Alexander Ahn, Mathieu Rouanne, Dylan L. Mariuzza, Tal Danino, Nicholas Arpaia

{"title":"Programmable bacteria synergize with PD-1 blockade to overcome cancer cell–intrinsic immune resistance mechanisms","authors":"Fangda Li, Zaofeng Yang, Thomas M. Savage, Rosa L. Vincent, Kenia de los Santos-Alexis, Alexander Ahn, Mathieu Rouanne, Dylan L. Mariuzza, Tal Danino, Nicholas Arpaia","doi":"10.1126/sciimmunol.adn9879","DOIUrl":"10.1126/sciimmunol.adn9879","url":null,"abstract":"<div >Interferon-γ (IFN-γ) is a potent cytokine critical for response to immunotherapy, yet conventional methods to systemically deliver this cytokine have been hindered by severe dose-limiting toxicities. Here, we engineered a strain of probiotic bacteria that home to tumors and locally release IFN-γ. A single intratumoral injection of these IFN-γ–producing bacteria was sufficient to drive systemic tumor antigen–specific antitumor immunity, without observable toxicity. Although cancer cells use various resistance mechanisms to evade immune responses, bacteria-derived IFN-γ overcame primary resistance to programmed cell death 1 (PD-1) blockade via activation of cytotoxic Foxp3<sup>−</sup>CD4<sup>+</sup> and CD8<sup>+</sup> T cells. Moreover, by activating natural killer (NK) cells, bacteria-derived IFN-γ also overcame acquired resistance mechanisms to PD-1 blockade, specifically loss-of-function mutations in IFN-γ signaling and antigen presentation pathways. Collectively, these results demonstrate the promise of combining IFN-γ–producing bacteria with PD-1 blockade as a therapeutic strategy for overcoming immunotherapy-resistant, locally advanced, and metastatic disease.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 100","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adn9879","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The acid-sensing receptor GPR65 on tumor macrophages drives tumor growth in obesity 肿瘤巨噬细胞上的酸感应受体 GPR65 推动肥胖症肿瘤的生长

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-18 DOI: 10.1126/sciimmunol.adg6453

Sreya Bagchi, Robert Yuan, Han-Li Huang, Weiruo Zhang, David Kung-Chun Chiu, Hyungjoo Kim, Sophia L. Cha, Lorna Tolentino, Joshua Lowitz, Yilin Liu, Anna Moshnikova, Oleg Andreev, Sylvia Plevritis, Edgar G. Engleman

引用次数: 0

An ILC2-chitinase circuit restores lung homeostasis after epithelial injury 上皮损伤后，ILC2-几丁质酶回路可恢复肺稳态

IF 17.6 1区医学

Science Immunology Pub Date : 2024-10-18 DOI: 10.1126/sciimmunol.adl2986

Haerin Jung, Do-Hyun Kim, Roberto Efraín Díaz, J. Michael White, Summer Rucknagel, Lauryn Mosby, Yilin Wang, Sanjana Reddy, Emma S. Winkler, Ahmed O. Hassan, Baoling Ying, Michael S. Diamond, Richard M. Locksley, James S. Fraser, Steven J. Van Dyken

{"title":"An ILC2-chitinase circuit restores lung homeostasis after epithelial injury","authors":"Haerin Jung, Do-Hyun Kim, Roberto Efraín Díaz, J. Michael White, Summer Rucknagel, Lauryn Mosby, Yilin Wang, Sanjana Reddy, Emma S. Winkler, Ahmed O. Hassan, Baoling Ying, Michael S. Diamond, Richard M. Locksley, James S. Fraser, Steven J. Van Dyken","doi":"10.1126/sciimmunol.adl2986","DOIUrl":"10.1126/sciimmunol.adl2986","url":null,"abstract":"<div >Environmental exposures increase the risk for severe lung disease, but specific drivers of persistent epithelial injury and immune dysfunction remain unclear. Here, we identify a feedback circuit triggered by chitin, a common component of airborne particles, that affects lung health after epithelial injury. In mice, epithelial damage disrupts lung chitinase activity, leading to environmental chitin accumulation, impaired epithelial renewal, and group 2 innate lymphoid cell (ILC2) activation. ILC2s, in turn, restore homeostasis by inducing acidic mammalian chitinase (AMCase) in regenerating epithelial cells and promoting chitin degradation, epithelial differentiation, and inflammatory resolution. Mice lacking AMCase or ILC2s fail to clear chitin and exhibit increased mortality and impaired epithelial regeneration after injury. These effects are ameliorated by chitinase replacement therapy, demonstrating that chitin degradation is crucial for recovery after various forms of lung perturbation. Thus, the ILC2-chitinase response circuit may serve as a target for alleviating persistent postinjury lung epithelial and immune dysfunction.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"9 100","pages":""},"PeriodicalIF":17.6,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0