Seminars in Immunopathology最新文献_第2页

The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions. 肾纤维化中的乳酸-乳酸化回路：从小管代谢重编程到巨噬细胞效应功能的细胞串扰。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-08-24 DOI: 10.1007/s00281-026-01083-y

Yiwei Shang, Yunguang Wang, Qikai Luo, Ran He, Shaoting Wang, Binqi Wang, Weiye Lin, Yourou Zhou, Qing He, Qiang He, Juan Jin

{"title":"The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.","authors":"Yiwei Shang, Yunguang Wang, Qikai Luo, Ran He, Shaoting Wang, Binqi Wang, Weiye Lin, Yourou Zhou, Qing He, Qiang He, Juan Jin","doi":"10.1007/s00281-026-01083-y","DOIUrl":"10.1007/s00281-026-01083-y","url":null,"abstract":"Kidney fibrosis is the histopathological endpoint of chronic kidney disease, yet antifibrotic trials targeting individual molecular nodes have repeatedly failed to translate into patient benefit. The pattern suggests that renal fibrosis is sustained by a recurrent circuit rather than a linear cascade. Here we propose a tubular-macrophage lactate-lactylation circuit that integrates tubular and macrophage evidence into a single cellular axis. Injured tubular cells reprogramme glycolytically and generate a sustained lactate-rich niche. On both sides of the tubulointerstitial interface, lactate is converted into histone and non-histone lactyl-lysine (Kla) marks that lock in profibrotic transcription, derange mitochondrial function and dampen innate immune surveillance. Macrophage outputs, profibrotic macrophage programmes, innate-immune memory, paracrine activation of fibroblasts/pericytes and, in selected contexts, macrophage-to-myofibroblast transition, feed back on tubular cells and the stromal compartment through bidirectional vesicular and cytokine signalling, generating the recurrent topology that distinguishes a circuit from a linear pathway. The supporting evidence is uneven across compartments; we stratify each key claim by tier of evidence and map the circuit onto current biomarker and therapeutic strategies. The framework clarifies why single-node interventions have not succeeded, and points to combinations that engage substrate supply, lactylation machinery, transcriptional output and intercellular feedback in parallel.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148814119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies. 哮喘的上皮免疫界面：驱动新治疗策略的机制见解。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-07-31 DOI: 10.1007/s00281-026-01079-8

Jingyi Deng, Jun Zhao, Wenlu Zhu, Yuanhui Li, Dexin Nie, Yuyu Zhong, Xinlong Lian, Suidong Ouyang

{"title":"Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.","authors":"Jingyi Deng, Jun Zhao, Wenlu Zhu, Yuanhui Li, Dexin Nie, Yuyu Zhong, Xinlong Lian, Suidong Ouyang","doi":"10.1007/s00281-026-01079-8","DOIUrl":"10.1007/s00281-026-01079-8","url":null,"abstract":"Asthma is a heterogeneous chronic respiratory syndrome driven by complex interactions between environmental triggers and the host immune system while biologic therapies targeting downstream type 2 cytokines (e.g., anti-IL-5, anti-IL-4Rα) have improved outcomes, the recent success of upstream epithelial-targeting agents like Tezepelumab highlights the potential of targeting disease at its source. Accordingly, recent conceptual advances have redefined the airway epithelium from a passive structural shield to an active immunometabolic hub. This review provides a concise synthesis of emerging mechanistic insights into how airway epithelial cells (AECs) orchestrate both innate and adaptive immune responses. We systematically map the bidirectional crosstalk between the epithelium and diverse immune populations, highlighting how metabolic reprogramming, vesicle-mediated intercellular communication, and neuro-immune circuitry act synergistically to sustain chronic airway inflammation. Furthermore, we explore how these dynamic networks dictate distinct asthma endotypes, ranging from classic type 2 to non-type 2 phenotypes. By delineating these underlying pathobiological mechanisms, this article underscores the translational potential of targeting upstream epithelial signaling. Ultimately, advancing our understanding of this epithelial-immune interface paves the way for emerging precision therapeutics aimed at modifying disease progression and restoring airway homeostasis.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148631572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PD-1⁺ CD8⁺ T cells: roles of PD-1 beyond an exhaustion marker. PD-1 + CD8 + T细胞：PD-1在衰竭标志物之外的作用

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-07-07 DOI: 10.1007/s00281-026-01078-9

Jingyi Chen, Zixiang Chen, Liangjie Xu, Jieting Jia, Ke Rui, Jie Tian

{"title":"PD-1⁺ CD8⁺ T cells: roles of PD-1 beyond an exhaustion marker.","authors":"Jingyi Chen, Zixiang Chen, Liangjie Xu, Jieting Jia, Ke Rui, Jie Tian","doi":"10.1007/s00281-026-01078-9","DOIUrl":"10.1007/s00281-026-01078-9","url":null,"abstract":"Programmed cell death protein 1 (PD-1) has long been considered a central molecule in CD8⁺ T cell exhaustion and immunosuppression. However, recent studies have revealed that PD-1⁺CD8⁺ T cells are not a homogeneous population of terminally dysfunctional cells, but rather constitute key immune cells with significant heterogeneity and functional plasticity within tissue immune microenvironments. PD-1 signaling operates throughout multiple stages of CD8⁺ T cell biology, including thymic development, peripheral activation, chronic antigen stimulation, and tissue residency. By finely regulating T cell receptors (TCRs) signal strength, metabolic state, and transcriptional programs, it deeply participates in cell fate decisions while limiting immunopathology. In chronic infections and tumors, persistent antigen stimulation drives PD-1⁺CD8⁺ T cells to form an exhaustion lineage with a defined differentiation hierarchy, encompassing stem-like precursor cells, effector-like transitional cells, and terminally exhausted cells. PD-1 is not only a characteristic marker of this lineage but also a critical regulatory node through which immune checkpoint blockade therapy exerts its therapeutic effects. Furthermore, in contexts such as tissue-resident memory T cells (TRM), GZMK⁺CD8⁺ T cells, and other disease-associated microenvironments, sustained PD-1 expression often represents an adaptive functional regulatory state rather than mere functional inhibition. This review explores the multidimensional regulatory roles of PD-1 in CD8⁺ T cells, with a focus on elucidating the diverse functions and clinical significance of PD-1⁺CD8⁺ T cells in cancer, chronic infections, and autoimmune diseases.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148397578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies. 炎症与雌激素在子宫腺肌症中的相互作用：从分子机制到治疗策略。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-06-08 DOI: 10.1007/s00281-026-01077-w

Feng Li, Huai Jian Wang, Yu Zhang, Feng Juan Nan, Li Xu, Zhi Yong Liu, Wei Shi

{"title":"The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.","authors":"Feng Li, Huai Jian Wang, Yu Zhang, Feng Juan Nan, Li Xu, Zhi Yong Liu, Wei Shi","doi":"10.1007/s00281-026-01077-w","DOIUrl":"10.1007/s00281-026-01077-w","url":null,"abstract":"Adenomyosis is a common and difficult disease in gynecology. Its main clinical manifestations include uterine hypertrophy, excessive menstruation, pelvic pain and infertility, which have a serious impact on women's health. Seriously affects women's health. At present, the pathogenesis of this disease is not clear; however, the increase in local estrogen and the occurrence of an inflammatory response are widely believed to be closely related to the development of adenomyotic lesions. Although progress has been made in understanding how estrogen and inflammation play their respective roles in adenomyosis, the relationship between estrogen and inflammation and its impact on adenomyosis are not fully understood. In this work, we summarize the effects of estrogen and inflammation on the occurrence and development of adenomyosis, including the involved biological processes and related signal transduction mechanisms, as well as the targeted drugs for clinical treatment, and further summarize the interactions between the two in adenomyosis as well as the available evidence for clinical applications. This review helps to broaden our understanding of the role of the vicious inflammatory‒estrogen cycle in the pathogenesis and pathophysiology of adenomyosis, and it provides new ideas for the treatment of uterine adenomyosis.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13246559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148199789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 complex of gut microbial metabolites and sex hormones in Alzheimer's disease. 阿尔茨海默病中肠道微生物代谢物和性激素的复合物。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-06-01 DOI: 10.1007/s00281-026-01076-x

Aisa Bahar, Meisam Khazaei, Hamed Tahmasebi

{"title":"The complex of gut microbial metabolites and sex hormones in Alzheimer's disease.","authors":"Aisa Bahar, Meisam Khazaei, Hamed Tahmasebi","doi":"10.1007/s00281-026-01076-x","DOIUrl":"10.1007/s00281-026-01076-x","url":null,"abstract":"Alzheimer's Disease (AD) is a progressive neurodegenerative disorder with a complex pathophysiological mechanism and a marked sex difference in prevalence and disease severity, with women being more affected and showing a more aggressive disease course. Recent studies indicate that a complex interplay among gut microbiota (GM), their metabolites, and sex hormones is a crucial factor in AD pathogenesis. In this review, we attempted to synthesize current studies to critically discuss the tripartite interplay among GM, sex hormones, and the brain in AD. Firstly, we discuss the role of the microbiota-gut-brain axis in AD pathogenesis with a focus on how gut dysbiosis contributes to neuroinflammation, disruption of the blood-brain barrier (BBB), and accumulation of pathological proteins. Then, we discuss the mechanistic roles of various GM-derived metabolites in AD pathogenesis, with a focus on the two-edged role of SCFAs and their derivatives, the neuroactive role of tryptophan and its derivatives, and the modulatory roles of bile acids and trimethylamine N-oxide. Finally, we discuss a novel concept, the \"microgenderome,\" referring to the bidirectional interplay between sex hormones and GM, and how GM regulates sex hormone levels through unique enzymatic functions termed the \"estrobolome\" and a newly proposed \"testobolome.\"","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148138937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Endometrial pathophysiology and pregnancy: from mechanism to intervention. 子宫内膜病理生理与妊娠：从机制到干预。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-05-19 DOI: 10.1007/s00281-026-01074-z

Lianghui Diao, Joanne Kwak-Kim

引用次数: 0

Advances in understanding the dual roles of testicular immune responses: From immune privilege to inflammation. 了解睾丸免疫反应的双重作用的进展：从免疫特权到炎症。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-05-12 DOI: 10.1007/s00281-026-01073-0

Xianglong Wang, Feng Jiang, Haijuan Yang, Dong Niu, Huaming Xi

{"title":"Advances in understanding the dual roles of testicular immune responses: From immune privilege to inflammation.","authors":"Xianglong Wang, Feng Jiang, Haijuan Yang, Dong Niu, Huaming Xi","doi":"10.1007/s00281-026-01073-0","DOIUrl":"10.1007/s00281-026-01073-0","url":null,"abstract":"The testis is an immune-privileged organ that balances protection of developing germ cells with the need to respond to pathogens. This review summarizes the dual nature of testicular immunity. A tolerogenic microenvironment is maintained through the blood-testis barrier (BTB) and immunomodulatory factors from Sertoli and Leydig cells, which suppress immune activation and preserve spermatogenesis. When infection, inflammation, or environmental stress disrupts this balance, immune responses shift toward pathology, inducing inflammatory cascades, apoptosis, and impaired fertility. We highlight the tightly regulated complement system, the plasticity and crosstalk of testicular immune cells-including macrophages, dendritic cells (DCs), T cells, and B cells-and the central role of the Toll-like receptor (TLR)-NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome-Reactive oxygen species (ROS) axis in mediating inflammation and cell death. Viral infections further induce remodeling of the BTB, perturb immune homeostasis, and contribute to the development of orchitis. Overall, testicular immunity exhibits both protective and pathogenic features, offering insights for targeted therapies in male reproductive immune disorders.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147875398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Climate change-associated heat extremes and immune dysregulation: emerging links with autoimmunity, allergy, and infectious diseases. 气候变化相关的极端高温和免疫失调：与自身免疫、过敏和传染病的新联系

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-05-11 DOI: 10.1007/s00281-026-01075-y

Paraskevi C Fragkou, Charalampos D Moschopoulos, Dominika Marová, Barrak Alahmad, Chrysanthi Skevaki

{"title":"Climate change-associated heat extremes and immune dysregulation: emerging links with autoimmunity, allergy, and infectious diseases.","authors":"Paraskevi C Fragkou, Charalampos D Moschopoulos, Dominika Marová, Barrak Alahmad, Chrysanthi Skevaki","doi":"10.1007/s00281-026-01075-y","DOIUrl":"10.1007/s00281-026-01075-y","url":null,"abstract":"Climate extremes are increasingly shaping both environmental and human health outcomes. Global warming has led to a rise in the frequency, duration, and intensity of extreme temperature events, with heatwaves emerging as one of the most hazardous weather-related threats. Beyond their well-recognized cardiovascular and respiratory effects, heat extremes are now understood to influence immune function. Growing evidence indicates that heat extremes along with air pollution, wildfires, humidity shifts, and ecosystem disruption can impair epithelial barrier integrity and disturb immune regulation. These stressors may promote chronic inflammation, alter adaptive immune responses, and compromise host defense mechanisms. Experimental and epidemiological data suggest that heat stress can reduce effective B-cell responses, modify antigen presentation, and increase inflammatory signaling, while combined exposures to heat and pollutants may further increase susceptibility to infectious, allergic, and autoimmune diseases. Although the physical drivers of climate change are well established, the biological pathways linking environmental stressors to immune dysregulation remain incompletely defined. This review synthesizes current evidence on the mechanisms by which extreme heat events influence immune tolerance and disease risk. We discuss implications for allergy, autoimmunity, and infectious diseases, highlight vulnerable populations, and outline key research priorities needed to inform clinical and public health adaptation.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147875432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The cancer-microbiome axis: Mechanisms and emerging therapeutic strategies. 癌症-微生物组轴：机制和新兴的治疗策略。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-04-16 DOI: 10.1007/s00281-026-01072-1

Maria Rae Walker, Marlene Schwarzfischer, Michael Scharl

{"title":"The cancer-microbiome axis: Mechanisms and emerging therapeutic strategies.","authors":"Maria Rae Walker, Marlene Schwarzfischer, Michael Scharl","doi":"10.1007/s00281-026-01072-1","DOIUrl":"10.1007/s00281-026-01072-1","url":null,"abstract":"The human microbiome has emerged as a critical modulator of cancer development, progression, and therapeutic response. Advances in sequencing and functional profiling have revealed that commensal microorganisms—particularly bacteria—interact closely with host immune and metabolic pathways, influencing tumor immunity across multiple cancer types. Dysbiosis of the gut microbiome has been associated with tumorigenesis, immune evasion, and resistance to therapy, while specific microbial taxa and metabolites have been shown to enhance antitumor immune responses. These discoveries have catalyzed the development of microbiome-based therapeutic strategies aimed at reshaping host–tumor interactions. This review summarizes current understanding of the cancer–microbiome axis, with a particular focus on therapeutic interventions that leverage microbial modulation. We discuss fecal microbiota transplantation (FMT) as an early, proof-of-concept approach demonstrating the capacity of the microbiome to restore responsiveness to immune checkpoint inhibitors, while also highlighting its limitations related to variability, standardization, and mechanistic uncertainty. We then examine emerging reductionist strategies, including supplementation with individual bacterial strains, defined consortia, and engineered microbes designed to deliver immunomodulatory payloads directly within the tumor microenvironment. Finally, we explore how microbial modulation interfaces with conventional cancer therapies such as chemotherapy, hormonal therapy, and cellular immunotherapies. Together, these studies illustrate a rapidly evolving field transitioning from correlative observations to mechanistically informed therapeutic design. While significant technical and biological challenges remain, continued integration of microbiology, immunology, and synthetic biology holds promise for translating microbiome-based interventions into safe, precise, and effective cancer therapies.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Cytokine-mediated, organ-specific immune modulation and dysregulation of innate lymphocytes in sepsis. 脓毒症中细胞因子介导的器官特异性免疫调节和先天淋巴细胞失调。

IF 11.5 2区医学

Seminars in Immunopathology Pub Date : 2026-04-10 DOI: 10.1007/s00281-026-01071-2

Seoyeon Han, Sejong Bae, Seungwon Ryu

{"title":"Cytokine-mediated, organ-specific immune modulation and dysregulation of innate lymphocytes in sepsis.","authors":"Seoyeon Han, Sejong Bae, Seungwon Ryu","doi":"10.1007/s00281-026-01071-2","DOIUrl":"10.1007/s00281-026-01071-2","url":null,"abstract":"Sepsis is a life-threatening condition that is marked by dysregulated host immune responses that can induce multiorgan dysfunction. Recent evidence suggests that this immunopathology involves tissue-resident innate lymphocytes, including innate-lymphoid cells (ILCs) and innate-like lymphocytes (ILLs). This review elucidates the organ-specific roles of the three ILC groups (ILC1s, ILC2s, and ILC3s) and two ILL types (NKT and γδ T cells) in sepsis, particularly their cytokine-mediated functions and cell-cell interactions. The literature shows that in the lungs, ILC2-derived IL-9 and IL-13 mitigate pulmonary inflammation and preserve endothelial integrity but dysregulated ILC2 activation may exacerbate injury. In the heart, ILC2s may mediate cardioprotective effects by inducing IL-13-STAT3 signaling and IL-5-mediated eosinophil recruitment. Kidney-resident ILC2s may promote tissue repair in acute-kidney injury (AKI) but their role in sepsis-associated AKI remains underexplored. In the gut and liver, ILC3s protect from sepsis via IL-22, which promotes barrier integrity, but they can convert into ILC1s, whose IFN-γ contributes to tissue damage. Circulating NK cells may play pathogenic and beneficial roles at different times after sepsis onset. NKT and γδ T cells are respectively protective and pathogenic in the gut and liver, likely through their respective production of IFN-γ and IL-17 A. Thus, ILCs and ILLs play key roles in sepsis and could be potential therapeutic targets. Further research is needed to elucidate their precise contributions in each organ and how time since onset and local and systemic conditions affect these contributions.","PeriodicalId":21704,"journal":{"name":"Seminars in Immunopathology","volume":"48 1","pages":""},"PeriodicalIF":11.5,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147646452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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