Cellular &Molecular Immunology最新文献_第2页

mRNA 3'UTR length matters: alternative polyadenylation shapes autophagy and inflammatory responses in macrophages. mRNA 3'UTR长度影响：可选择的多聚腺苷化影响巨噬细胞的自噬和炎症反应。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-17 DOI: 10.1038/s41423-024-01252-9

Wenjun Cai, Emiliano P Ricci

引用次数: 0

Increasing evidence for the pathogenic role of keratinocytes in lupus. 越来越多的证据表明角化细胞在狼疮中的致病作用。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-17 DOI: 10.1038/s41423-024-01254-7

Benjamin Klein, Allison C Billi, J Michelle Kahlenberg

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Author Correction: A special RELationship between sugar and tumor-infiltrating regulatory T cells. 作者更正：糖与肿瘤浸润调节性T细胞之间的特殊关系。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-16 DOI: 10.1038/s41423-025-01256-z

Ingo Schmitz

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Author Correction: A spike protein S2 antibody efficiently neutralizes the Omicron variant. 作者更正：刺突蛋白S2抗体有效地中和了Omicron变体。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-16 DOI: 10.1038/s41423-025-01255-0

Jia Hu, Xiang Chen, Xingbing Lu, Lijuan Wu, Liyuan Yin, Lingling Zhu, Hao Liang, Feng Xu, Qinghua Zhou

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Myelin debris as an initiator of microglial dysfunction and neuropathology in Alzheimer’s disease 髓磷脂碎片作为阿尔茨海默病小胶质细胞功能障碍和神经病理学的启动器。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-14 DOI: 10.1038/s41423-024-01243-w

Joshua D. Samuels, John R. Lukens

引用次数: 0

Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer’s disease 脱髓鞘源性溶磷脂酰丝氨酸促进阿尔茨海默病小鼠模型中的小胶质功能障碍和神经病理学。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-01 DOI: 10.1038/s41423-024-01235-w

Yubo Zhou, Zonghui Huang, Bolong Lin, Ming Ma, Yize Hao, Juanjuan Liu, Wen Xu, Guangming Huang, Wei Mo, Xiaqiong Wang, Wei Jiang, Rongbin Zhou

{"title":"Demyelination-derived lysophosphatidylserine promotes microglial dysfunction and neuropathology in a mouse model of Alzheimer’s disease","authors":"Yubo Zhou, Zonghui Huang, Bolong Lin, Ming Ma, Yize Hao, Juanjuan Liu, Wen Xu, Guangming Huang, Wei Mo, Xiaqiong Wang, Wei Jiang, Rongbin Zhou","doi":"10.1038/s41423-024-01235-w","DOIUrl":"10.1038/s41423-024-01235-w","url":null,"abstract":"Microglia dysfunction-associated neuroinflammation is an important driver of Alzheimer’s disease (AD), but the mechanism is poorly understood. Here, we show that demyelination promotes neuroinflammation and cognitive impairment via the lysophosphatidylserine (LysoPS)-GPR34 axis in AD. Demyelination is observed at the early stage and is accompanied by an increase in LysoPS in myelin debris in a 5xFAD mouse model of AD. Reducing the content of LysoPS in myelin or inhibiting its receptor GPR34 via genetic or pharmacological approaches can reduce microglial dysfunction and neuroinflammation and improve microglial Aβ phagocytosis, subsequently resulting in less Aβ deposition and memory restoration in 5xFAD mice. Furthermore, increased LysoPS production and microglial GPR34 expression were also observed in the brains of AD patients. These results reveal the pathogenic role of demyelination-derived LysoPS in microglial dysfunction and AD pathology and suggest that blocking GPR34 as a therapeutic strategy beyond targeting Aβ.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"22 2","pages":"134-149"},"PeriodicalIF":21.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909156","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

NRP1 instructs IL-17-producing ILC3s to drive colitis progression NRP1指示产生il -17的ilc3驱动结肠炎的进展。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-01 DOI: 10.1038/s41423-024-01246-7

Ying Wang, Jianye Wang, Gaoyu Liu, Xianfu Yi, Jingyi Wu, Hailong Cao, Lijuan Zhang, Pan Zhou, Yong Fan, Ying Yu, Qiang Liu, Zhi Yao, Haitao Wang, Jie Zhou

{"title":"NRP1 instructs IL-17-producing ILC3s to drive colitis progression","authors":"Ying Wang, Jianye Wang, Gaoyu Liu, Xianfu Yi, Jingyi Wu, Hailong Cao, Lijuan Zhang, Pan Zhou, Yong Fan, Ying Yu, Qiang Liu, Zhi Yao, Haitao Wang, Jie Zhou","doi":"10.1038/s41423-024-01246-7","DOIUrl":"10.1038/s41423-024-01246-7","url":null,"abstract":"Group 3 innate lymphoid cells (ILC3s) control tissue homeostasis and orchestrate mucosal inflammation; however, the precise mechanisms governing ILC3 activity are fully understood. Here, we identified the transmembrane protein neuropilin-1 (NRP1) as a positive regulator of interleukin (IL)-17-producing ILC3s in the intestine. NRP1 was markedly upregulated in intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) compared with healthy controls. Genetic deficiency of NRP1 reduces the frequency of ILC3s in the gut and impairs their production of IL-17A in an NF-κB signaling-dependent and cell-intrinsic manner. The diminished IL-17A production in ILC3s altered the composition of the microbiota and improved the outcome of dextran sodium sulfate (DSS)-induced colitis. Furthermore, pharmacological inhibition of NRP1 with EG00229 alleviated the severity of colitis. These observations demonstrated the critical role of NRP1 in the control of intestinal ILC3s, suggesting that NRP1 is a potential therapeutic target for IBD.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"22 2","pages":"161-175"},"PeriodicalIF":21.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909159","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

Sequential STING and CD40 agonism drives massive expansion of tumor-specific T cells in liposomal peptide vaccines 序列STING和CD40激动作用驱动脂质体肽疫苗中肿瘤特异性T细胞的大量扩增。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-01-01 DOI: 10.1038/s41423-024-01249-4

Dmitrij Ostroumov, Naomi Benne, Fernando Lozano Vigario, Oscar Escalona-Rayo, Ksenia Dodz, Sarah Sauer, Lena Luisa Suhl, Hans Heiner Wedemeyer, Florian Kühnel, Bram Slütter, Thomas Christian Wirth

{"title":"Sequential STING and CD40 agonism drives massive expansion of tumor-specific T cells in liposomal peptide vaccines","authors":"Dmitrij Ostroumov, Naomi Benne, Fernando Lozano Vigario, Oscar Escalona-Rayo, Ksenia Dodz, Sarah Sauer, Lena Luisa Suhl, Hans Heiner Wedemeyer, Florian Kühnel, Bram Slütter, Thomas Christian Wirth","doi":"10.1038/s41423-024-01249-4","DOIUrl":"10.1038/s41423-024-01249-4","url":null,"abstract":"The clinical use of cancer vaccines is hampered by the low magnitude of induced T-cell responses and the need for repetitive antigen stimulation. Here, we demonstrate that liposomal formulations with incorporated STING agonists are optimally suited to deliver peptide antigens to dendritic cells in vivo and to activate dendritic cells in secondary lymphoid organs. One week after liposomal priming, systemic administration of peptides and a costimulatory agonistic CD40 antibody enables ultrarapid expansion of T cells, resulting in massive expansion of tumor-specific T cells in the peripheral blood two weeks after priming. In the MC-38 colon cancer model, this synthetic prime-boost regimen induces rapid regression and cure of large established subcutaneous cancers via the use of a single tumor-specific neoantigen. These experiments demonstrate the feasibility of liposome-based heterologous vaccination regimens to increase the therapeutic efficacy of peptide vaccines in the context of immunogenic adjuvants and costimulatory booster immunizations. Our results provide a rationale for the further development of modern liposomal peptide vaccines for cancer therapy.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"22 2","pages":"150-160"},"PeriodicalIF":21.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11782543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909161","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

A special RELationship between sugar and tumor-infiltrating regulatory T cells. 糖与肿瘤浸润调节性T细胞的特殊关系。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-12-17 DOI: 10.1038/s41423-024-01248-5

Ingo Schmitz

引用次数: 0

MYO1F regulates T-cell activation and glycolytic metabolism by promoting the acetylation of GAPDH MYO1F通过促进GAPDH乙酰化调节t细胞活化和糖酵解代谢。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2024-12-13 DOI: 10.1038/s41423-024-01247-6

Zhihui Cui, Heping Wang, Xiong Feng, Chuyu Wu, Ming Yi, Ruirui He, Ting Pan, Ru Gao, Lingyun Feng, Bo Zeng, Guoling Huang, Yuan Wang, Yanyun Du, Cun-jin Zhang, Xue Xiao, Chenhui Wang

{"title":"MYO1F regulates T-cell activation and glycolytic metabolism by promoting the acetylation of GAPDH","authors":"Zhihui Cui, Heping Wang, Xiong Feng, Chuyu Wu, Ming Yi, Ruirui He, Ting Pan, Ru Gao, Lingyun Feng, Bo Zeng, Guoling Huang, Yuan Wang, Yanyun Du, Cun-jin Zhang, Xue Xiao, Chenhui Wang","doi":"10.1038/s41423-024-01247-6","DOIUrl":"10.1038/s41423-024-01247-6","url":null,"abstract":"Proper cellular metabolism in T cells is critical for a productive immune response. However, when dysregulated by intrinsic or extrinsic metabolic factors, T cells may contribute to a wide spectrum of diseases, such as cancers and autoimmune diseases. However, the metabolic regulation of T cells remains incompletely understood. Here, we show that MYO1F is required for human and mouse T-cell activation after TCR stimulation and that T-cell-specific Myo1f knockout mice exhibit an increased tumor burden and attenuated EAE severity due to impaired T-cell activation in vivo. Mechanistically, after TCR stimulation, MYO1F is phosphorylated by LCK at tyrosines 607 and 634, which is critical for glyceraldehyde-3-phosphate dehydrogenase (GAPDH) acetylation at Lys84, 86 and 227 mediated by α-TAT1, which is an acetyltransferase, and these processes are important for its activation, cellular glycolysis and thus the effector function of T cells. Importantly, we show that a fusion protein of VAV1-MYO1F, a recurrent peripheral T-cell lymphoma (PTCL)-associated oncogenic protein, promotes hyperacetylation of GAPDH and its activation, which leads to aberrant glycolysis and T-cell proliferation, and that inhibition of the activity of GAPDH significantly limits T-cell activation and proliferation and extends the survival of hVAV1-MYO1F knock-in mice. Moreover, hyperacetylation of GAPDH was confirmed in human PTCL patient samples containing the VAV1-MYO1F gene fusion. Overall, this study revealed not only the mechanisms by which MYO1F regulates T-cell metabolism and VAV1-MYO1F fusion-induced PTCL but also promising therapeutic targets for the treatment of PTCL.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"22 2","pages":"176-190"},"PeriodicalIF":21.8,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817420","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