International immunology最新文献

Immunological memory in natural killer cells. 自然杀伤细胞的免疫记忆。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-22 DOI: 10.1093/intimm/dxaf016

Tsukasa Nabekura

{"title":"Immunological memory in natural killer cells.","authors":"Tsukasa Nabekura","doi":"10.1093/intimm/dxaf016","DOIUrl":"10.1093/intimm/dxaf016","url":null,"abstract":"Immune cells are classified into adaptive and innate immune cells. Adaptive immune cells-i.e. T cells and B cells-respond to pathogens in an antigen-specific manner and then provide immunological memory, contributing to long-term host defense against reinfection. In contrast, innate immune cells promptly respond to pathogens, but they are short-lived and have been thought not to contribute to immunological memory. Natural killer (NK) cells are lymphocytes essential for controlling viral infections and cancer. NK cells-which have traditionally been classified as innate immune cells-have recently been revealed as being capable of differentiating into memory NK cells, thus participating in immunological memory, formerly considered to be restricted to adaptive immune cells. Like memory T and B cells, memory NK cells (i) can be long-lived; (ii) display distinct phenotypes from naïve and activated NK cells; (iii) show augmented cellular functions, as compared with naïve NK cells; (iv) have secondary proliferation capacity; and (v) confer an improved host defense when transferred to naïve recipients. Therefore, at least in a broad sense, they fulfill the definition of immunological memory. In this article, I provide an overview of NK cell memory and recent research trends regarding this phenomenon.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"435-443"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

B10 cells promote pro-resolving macrophage function through direct cell-cell contact and IL-10 secretion in Raw 264.7 cells. 在Raw 264.7细胞中，B10细胞通过细胞间的直接接触和IL-10的分泌，促进巨噬细胞的促溶解功能。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-22 DOI: 10.1093/intimm/dxaf012

Takumi Memida, Elaheh Dalir Abdolahinia, Guoqin Cao, Sunniva Ruiz, Shengyuan Huang, Satoru Shindo, Shin Nakamura, Jiang Lin, Toshihisa Kawai, Xiaozhe Han

{"title":"B10 cells promote pro-resolving macrophage function through direct cell-cell contact and IL-10 secretion in Raw 264.7 cells.","authors":"Takumi Memida, Elaheh Dalir Abdolahinia, Guoqin Cao, Sunniva Ruiz, Shengyuan Huang, Satoru Shindo, Shin Nakamura, Jiang Lin, Toshihisa Kawai, Xiaozhe Han","doi":"10.1093/intimm/dxaf012","DOIUrl":"10.1093/intimm/dxaf012","url":null,"abstract":"It is well known that regulatory B cells (Breg), especially IL-10-producing regulatory cells (B10), play an important role in immune regulation during inflammatory and infectious diseases. Although it has been revealed that the immune regulatory function of B10 can be exerted through cognate cell-cell contact with T cells, more research is needed to delineate its impact on other key cellular immune components within the immune microenvironment. In this study, we evaluated the effect of B10 on the phenotypic change of macrophages and their pro-resolving functional activities using various co-culture systems. The roles of cell-cell contact and the IL-10 secretion by B10 on macrophage differentiation and function were determined. Splenocyte-derived B10 cells from wild-type or IL-10 knockout (KO) mice were co-cultured with RAW 264.7 cells in the presence or absence of trans-well inserts. Macrophage polarization, programmed cell death 1 (PD-1) expression, production of specialized pro-resolving mediators (SPMs), and phagocytic activity were evaluated. The results showed that direct B10-macrophage co-culture enhanced the macrophage polarization towards a pro-resolving phenotype and their PD-1 expression, which was diminished when the cultured B10 and macrophages were separated by trans-well inserts, or when B cells from IL-10 KO mice were used for the co-culture. In addition, B10 was found to promote the release of specific SPM [resolvin D series 5 (RvD5)] and phagocytic activity by macrophages after co-culture. These effects were compromised in trans-well co-culture or co-cultures with IL-10-deficient B cells. Our results suggest that B10 promotes pro-resolving macrophage differentiation and function through direct cell-cell contact and IL-10 secretion.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"457-474"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Tertiary lymphoid structures: chronic inflammatory microenvironments in kidney diseases. 三级淋巴样结构：肾脏疾病的慢性炎症微环境。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-22 DOI: 10.1093/intimm/dxaf017

Takahisa Yoshikawa, Motoko Yanagita

{"title":"Tertiary lymphoid structures: chronic inflammatory microenvironments in kidney diseases.","authors":"Takahisa Yoshikawa, Motoko Yanagita","doi":"10.1093/intimm/dxaf017","DOIUrl":"10.1093/intimm/dxaf017","url":null,"abstract":"Chronic kidney disease is a global health problem with high morbidity and mortality rates. Acute kidney injury substantially increases the risk of chronic kidney disease progression, particularly in the elderly, partly because of prolonged inflammation that exacerbates kidney fibrosis and dysfunction. Tertiary lymphoid structures (TLSs) are ectopic lymphoid aggregates that develop in non-lymphoid organs during chronic inflammation, such as autoimmune diseases, cancers, and age-related inflammation. Age-dependent TLS formation is observed in various organs, such as the kidneys, bladder, lacrimal glands, and liver, potentially contributing to age-related disorders, including chronic kidney disease progression after acute kidney injury. TLSs contain heterogeneous cell populations, such as T cells, B cells, pro-inflammatory fibroblasts, and blood and lymphatic vessels, which orchestrate TLS development and expansion through intensive cell-cell interactions. Pro-inflammatory fibroblasts within TLSs drive TLS formation by producing various chemokines and cytokines that recruit and activate immune cells. Additionally, the CD153-CD30 signaling pathway between senescence-associated T cells and age-associated B cells, both of which increase with age, are essential for renal TLS maturation and expansion, which could be a promising therapeutic target in kidney injury in aged individuals. TLSs also develop in human kidney diseases, such as various glomerulopathies, transplanted kidneys, and renal cell carcinomas, thereby influencing patient outcomes. This review highlights the recent advances in our understanding of the cellular and molecular mechanisms underlying TLS development and pathogenicity, with a focus on age-dependent TLSs in the kidneys. Furthermore, the clinical relevance of TLSs in human kidney diseases is discussed.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"445-455"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143700222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Proteasome dysfunction in T cells causes immunodeficiency via cell cycle disruption and apoptosis. T细胞中的蛋白酶体功能障碍通过细胞周期破坏和细胞凋亡导致免疫缺陷。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-22 DOI: 10.1093/intimm/dxaf021

Erkhembayar Shinebaatar, Junko Morimoto, Rinna Koga, Thanh Nam Nguyen, Yuki Sasaki, Shigenobu Yonemura, Hidetaka Kosako, Koji Yasutomo

{"title":"Proteasome dysfunction in T cells causes immunodeficiency via cell cycle disruption and apoptosis.","authors":"Erkhembayar Shinebaatar, Junko Morimoto, Rinna Koga, Thanh Nam Nguyen, Yuki Sasaki, Shigenobu Yonemura, Hidetaka Kosako, Koji Yasutomo","doi":"10.1093/intimm/dxaf021","DOIUrl":"10.1093/intimm/dxaf021","url":null,"abstract":"Proteasomes are essential molecular complexes that regulate intracellular protein homeostasis by selectively degrading ubiquitinated proteins. Genetic mutations in proteasome subunits lead to proteasome-associated autoinflammatory syndromes (PRAAS) characterized by autoinflammation, partial progressive lipodystrophy, and, in certain cases, immunodeficiency. However, the molecular mechanisms by which proteasome dysfunction results in these phenotypes remain unclear. Here, we established a mouse model carrying a mutation in β5i (encoded by Psmb8) along with T-cell-specific β5 (encoded by Psmb5) deficiency (KIKO mice). The KIKO mice presented severe loss of mature T cells in the spleen but not in the thymus, with reduced proteasome activity leading to the accumulation of ubiquitinated proteins. The CD4+ T cells of KIKO mice presented impaired proliferative activity with cell cycle arrest in the G0/G1 phase following T cell receptor (TCR) engagement. T cells from KIKO mice underwent rapid cell death through apoptosis, as treatment of T cells with the caspase inhibitor Z-Val-Ala-Asp(Ome)-fluoromethylketone (Z-VAD-FMK) rescued cell viability. Moreover, proteasome dysfunction induced apoptosis in T cells without affecting either mitochondrial functions or endoplasmic reticulum (ER) stress responses. Thus, our data provide insight into the molecular mechanisms underlying not only immunodeficiency in PRAAS patients but also T-cell deficiency associated with other disorders.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"493-505"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12284234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Single-cell multiomic analysis revealed the differentiation, localization, and heterogeneity of IL10+ Foxp3- follicular T cells in humans. 单细胞多组学分析揭示了人体内IL10+ Foxp3-滤泡T细胞的分化、定位和异质性。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-22 DOI: 10.1093/intimm/dxaf014

Shusei Fujioka, Mayu Fujioka, Yusuke Imoto, Yasuyo Harada, Hiroyuki Yoshitomi, Masato Kubo, Yasuaki Hiraoka, Hideki Ueno

{"title":"Single-cell multiomic analysis revealed the differentiation, localization, and heterogeneity of IL10+ Foxp3- follicular T cells in humans.","authors":"Shusei Fujioka, Mayu Fujioka, Yusuke Imoto, Yasuyo Harada, Hiroyuki Yoshitomi, Masato Kubo, Yasuaki Hiraoka, Hideki Ueno","doi":"10.1093/intimm/dxaf014","DOIUrl":"10.1093/intimm/dxaf014","url":null,"abstract":"Germinal center (GC) reactions are tightly regulated to generate high-affinity antibodies. Although IL10+ Foxp3- follicular T cells have recently been described as contributing to the suppression of GC reactions, their differentiation, localization, and heterogeneity remain incompletely understood. Additionally, it remains unclear whether IL10+ Foxp3- follicular T cells represent a transient status or an independent subset. To address these gaps, we performed integrative single-cell analysis of transcriptomes, epigenomes, surface proteomes, and TCR repertoires in human tonsillar CD4+ T cells. Unbiased clustering revealed IL10+ Foxp3- follicular T cells as a transcriptionally and epigenetically unique subset. This subset exhibited features of both T follicular helper (Tfh) and T regulatory type 1 (Tr1) cells, and accordingly, hereafter, we call them T follicular regulatory type 1 (Tfr1) cells. Analysis using imaging mass cytometry and spatial RNA-TCR sequencing demonstrated their presence within GCs in humans. Bioinformatic analysis suggested that Tfr1 cells differentiate from GC-Tfh cells upon strong TCR stimulation, a finding corroborated by mouse in vivo experiments and time-series single-cell RNA-TCR sequencing of human in vivo CD4+ T cells. Of note, our bioinformatic analysis suggested that Tfr1 cells receive strong TCR signals from ICOS-Lhigh GC-B cells, likely representing high-affinity GC-B cells. Finally, we show that Tfr1 cells acquire a resident memory phenotype following an effector phase. Together, our findings suggest that high-affinity ICOS-Lhigh GC-B cells transform follicular T cells from GC-Tfh cells to Tfr1 cells, which likely become memory cells and reside in the lymphoid organ to support effective antibody production.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":"475-491"},"PeriodicalIF":4.8,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Interleukin-35 regulates the differentiation of regulatory T cells through the JAK-STAT pathway and influences glutamine metabolism in ARDS. 白细胞介素-35通过JAK-STAT通路调控调节性T细胞的分化，影响ARDS患者谷氨酰胺代谢。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-11 DOI: 10.1093/intimm/dxaf041

Qiao-Zhi Peng, Mu Zhang, Ai-Ping Zhang, Min-Kang Guo, Ren-Jie Luo, Ling Zeng, Chang Chen, Shi-Hui Lin, Fang Xu, Ke Xie

{"title":"Interleukin-35 regulates the differentiation of regulatory T cells through the JAK-STAT pathway and influences glutamine metabolism in ARDS.","authors":"Qiao-Zhi Peng, Mu Zhang, Ai-Ping Zhang, Min-Kang Guo, Ren-Jie Luo, Ling Zeng, Chang Chen, Shi-Hui Lin, Fang Xu, Ke Xie","doi":"10.1093/intimm/dxaf041","DOIUrl":"https://doi.org/10.1093/intimm/dxaf041","url":null,"abstract":"The aim of this study was to elucidate the effect of IL-35 on T cell differentiation and its mechanism. We evaluated the therapeutic effect of IL-35 on acute respiratory distress syndrome (ARDS) using clinical samples and mouse cecum ligation and puncture (CLP) model. The effects of IL-35 on Regulatory T cells (Treg) were verified by flow cytometry, immunohistochemistry (IHC) and qRT-PCR. Liquid chromatography-mass spectrometry (LC-MS) was used to detect the effects of IL-35 on changes in glutamin metabolites and TCA circulation. Western blot was used to detect changes in forkhead box protein 3 (Foxp3), key enzymes and STAT phosphorylation subgroup proteins in the presence of cerdulatinib. Finally, A549 cells were treated with EL-4 cell supernatant to explore the effect of cerdulatinib on the therapeutic effect of IL-35 injury. Inflammatory factors decreased and Foxp3 increased in response to IL-35. In addition, Foxp3 was upregulated in a glutamine-deficient environment, and notably, glutamine-related metabolism and TCA cycle-related substances were altered with the involvement of IL-35. IL-35 upregulated phosphorylation of STAT isoforms, and cerdulatinib reversed it. Finally, the effects of IL-35 on Foxp3, key enzymes and glutamine metabolite changes were all reversed by cerdulatinib. Our study shows that IL-35 reduces lung inflammation and promotes Treg differentiation. IL-35 affects the glutamine metabolism and the TCA cycle. In addition, we demonstrated that the relevant functions of IL-35 may be mediated by STAT isoform phosphorylation.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

TREX1 exonuclease in immunity and disease. TREX1外切酶在免疫和疾病中的作用。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-08 DOI: 10.1093/intimm/dxaf037

Zehua Shang, Lei Wang, Wen Zhou

引用次数: 0

Epigenomic Control of Immunity: From Mechanisms to Therapeutic Targets in Inflammatory Bowel Diseases. 免疫的表观基因组控制：从炎症性肠病的机制到治疗靶点。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-08 DOI: 10.1093/intimm/dxaf039

Han-Yu Shih, Giuseppe Sciumè, Yohei Mikami

{"title":"Epigenomic Control of Immunity: From Mechanisms to Therapeutic Targets in Inflammatory Bowel Diseases.","authors":"Han-Yu Shih, Giuseppe Sciumè, Yohei Mikami","doi":"10.1093/intimm/dxaf039","DOIUrl":"https://doi.org/10.1093/intimm/dxaf039","url":null,"abstract":"This review presents an overview of the emerging roles of epigenomic regulation in immune cell function, with a particular focus on its relevance in inflammatory bowel disease (IBD). Epigenetic mechanisms, including DNA methylation, histone modification, chromatin remodeling, and non-coding RNAs, are essential in directing immune cell development, activation, and lineage commitment. Advances in genomics and epigenomics have highlighted the dynamic nature of gene regulation as the cornerstone of immune homeostasis and adaptability. We summarize recent insights into enhancer dynamics, three-dimensional chromatin architecture, transcription factor signaling, and microRNA (miRNA)-mediated regulation that reshape our understanding of immune-mediated diseases. These findings not only deepen our knowledge of disease pathogenesis but also offer promising targets for therapeutic intervention. In this context, miRNAs have emerged as key post-transcriptional regulators with significant diagnostic and therapeutic potential for IBD. The field of immune epigenomics is advancing rapidly, offering powerful tools for dissecting complex immune responses and guiding the development of precise therapies for chronic inflammatory conditions.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

All-trans Retinoic Acid Suppresses IL-4 and IL-13 production in Th2 cells by modulating the nuclear receptor RARα, and Gfi1. 全反式维甲酸通过调节核受体RARα和Gfi1抑制Th2细胞中IL-4和IL-13的产生。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-02 DOI: 10.1093/intimm/dxaf040

Biswajit Biswas, Sayantee Hazra, Supratik Nandan, Shagnik Chattopadhyay, Swayam Prava Mansingh, Ritobrata Goswami

{"title":"All-trans Retinoic Acid Suppresses IL-4 and IL-13 production in Th2 cells by modulating the nuclear receptor RARα, and Gfi1.","authors":"Biswajit Biswas, Sayantee Hazra, Supratik Nandan, Shagnik Chattopadhyay, Swayam Prava Mansingh, Ritobrata Goswami","doi":"10.1093/intimm/dxaf040","DOIUrl":"https://doi.org/10.1093/intimm/dxaf040","url":null,"abstract":"All-trans retinoic acid (atRA), the bioactive component of vitamin A, plays a pivotal role in various biological processes. atRA, essential for embryonic development and immune functions, primarily mediates its regulatory effects by interacting with the nuclear receptor RARα. atRA-bound RARα enters the nucleus and forms a heterodimer with RXR. This heterodimer can then interact with various transcription factors to form regulatory complexes that influence gene expression. While the role of atRA in regulating the type 2 immune response has been studied, further exploration into its specific involvement in Th2 cell differentiation is necessary to fully elucidate underlying mechanisms and assess its therapeutic potential. Our study shows that atRA suppressed Th2 phenotype by down-regulating type 2 transcription factors such as Spi1 and cMaf, without altering Gata3 expression. atRA also reduced IL-4 and IL-13 production, while enhancing IL-5 expression, potentially through up-regulation of Gfi1. atRA increased the Gfi1 recruitment to the Il4 and Il13 promoters, along with the common enhancer Ecr. RARα, which is typically an inducer of Il4 and Il13, was observed to decrease recruitment to these loci in atRA-treated Th2 cells. Comparative gene expression analysis revealed a reduction in inflammatory responses in atRA-treated Th2 cells. Furthermore, these cells exhibited a negative correlation with epigenetic modifications, and nuclear receptor activity among other biological processes. Collectively, our findings suggest that atRA can effectively suppress the Th2 phenotype in vitro, through the regulation of key type 2 transcription factors and pathways, indicating its potential therapeutic implications for limiting type 2 immune responses.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy. 粪便微生物群移植用于免疫调节：改善溃疡性结肠炎和增强癌症免疫治疗。

IF 4.8 4区医学

International immunology Pub Date : 2025-07-02 DOI: 10.1093/intimm/dxaf038

Xiaochen Zhang, Dai Ishikawa, Akihito Nagahara

{"title":"Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy.","authors":"Xiaochen Zhang, Dai Ishikawa, Akihito Nagahara","doi":"10.1093/intimm/dxaf038","DOIUrl":"https://doi.org/10.1093/intimm/dxaf038","url":null,"abstract":"The gut microbiota plays an integral role in maintaining health and regulating various host functions, including immune responses. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach to restore gut microbial balance. Although widely recognized for its efficacy in treating ulcerative colitis (UC), FMT is now being investigated as an adjuvant therapy to enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment. This review summarizes the clinical applications of FMT in UC treatment and its potential role in cancer immunotherapy. FMT exhibits varying degrees of efficacy in the treatment of UC, with differences in outcomes attributed to variations in administration methods and donor selection. In cancer therapy, FMT has demonstrated the potential to improve ICI responses, particularly in patients with melanoma. However, its effects on other cancers remain unclear. Although FMT holds promise for UC and cancer immunotherapy, challenges such as inconsistent clinical outcomes and methodological variations persist. Standardized protocols and mechanistic studies are crucial to optimize FMT-based therapeutic strategies, and further research is required to establish its efficacy under diverse clinical conditions.","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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