Journal of Leukocyte Biology最新文献

{"title":"AML1-ETO and CCND2 overexpression cooperate to drive acute myeloid leukemia initiation and progression.","authors":"Junli Mou, Qianqian Huang, Xiaoyu Liu, Wenbing Liu, Yu Liu, Yihan Mei, Runxia Gu, Yingxi Xu, Kejing Tang, Zheng Tian, Haiyan Xing, Qing Rao, Min Wang, Shaowei Qiu, Jianxiang Wang","doi":"10.1093/jleuko/qiaf072","DOIUrl":"10.1093/jleuko/qiaf072","url":null,"abstract":"<p><p>Increasing numbers of clinical cohorts have detected CCND2 mutations in acute myeloid leukemia, especially in the subtype of acute myeloid leukemia with the t(8;21) translocation. This acute myeloid leukemia subtype is characterized by the formation of the AML1-ETO fusion gene. However, the AML1-ETO fusion gene alone is not sufficient to drive leukemia development. Additional mutations are required for leukemogenesis. In this study, we aim to investigate whether mutated CCND2 can cooperate with the AML1-ETO fusion gene to drive leukemia initiation and progression. In our previous study, the conditional AML1-ETO knock-in mouse model (AML1-ETO mouse), which represented a preleukemia stage as a myeloproliferative neoplasm phenotype, was established. To confirm whether the AML1-ETO and CCND2 mutation can cooperate to drive leukemia, the mice transduction and transplantation model harboring both AML1-ETO and CCND2 genes (both wild-type and mutant) was established. Upon the assessment of the phenotype, biological features, and survival of the mice, only the mice overexpressing AML1-ETO and CCND2 simultaneously eventually progressed to leukemia. Besides, compared to mice overexpressing the AML-ETO gene alone, mTOR and cell cycle-related pathways were significantly enriched in mice harboring both AML1-ETO and CCND2. The selective mTOR inhibitor everolimus can also reduce the leukemia burden and prolong the survival of this group of mice. In conclusion, it was confirmed that the introduction of the CCND2 gene into the AML/ETO preleukemia mice could trigger the development of leukemia. It was also confirmed that CCND2 overexpression resulted in the upregulation of the mTOR pathway, and inhibiting the pathway might be a therapeutic strategy for this subtype of leukemia.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"117 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Transgenic αβ TCR tonic signaling is leukemogenic while strong stimulation is leukemia suppressive.","authors":"","doi":"10.1093/jleuko/qiaf075","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf075","url":null,"abstract":"","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"117 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detrimental roles of innate immune cells in neuromyelitis optica spectrum disorder: Pathogenesis and therapeutic targeting.","authors":"Kar Min Loh, Yi Ying Cheok, Ting Fang Tang, Chung Yeng Looi, Won Fen Wong, Suhailah Abdullah","doi":"10.1093/jleuko/qiaf068","DOIUrl":"10.1093/jleuko/qiaf068","url":null,"abstract":"<p><p>Neuromyelitis optica spectrum disorder (NMOSD) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) that primarily affects the optic nerves, spinal cord, and brainstem, leading to severe relapses and potentially significant neurological disability. Most NMOSD patients present with anti-aquaporin-4 autoantibodies (AQP4-IgG), which trigger acute neuroinflammation and astrocyte damage through classical complement pathway activation and immune cell recruitment, yet AQP4-IgG alone does not fully account for NMOSD pathogenesis, suggesting additional contributing mechanisms. Emerging evidence highlights the critical role of innate immune cells-macrophages, neutrophils, eosinophils, and natural killer cells-in NMOSD lesion development, in which they amplify inflammation through cytokine release, antibody-dependent cellular cytotoxicity, and immune cell recruitment, ultimately exacerbating CNS damage. Importantly, recent advancements in NMOSD therapies have incorporated targeting innate immune responses, including interleukin-6 and complement inhibitors, and neutrophil and eosinophil modulators, enhancing treatment efficacy. This review explores the multifaceted roles of innate immune cells, their interactions with AQP4-IgG, and their contribution to disease progression. In summary, targeting innate immune pathways offers an alternative strategy to mitigate inflammation and damage in CNS.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078569","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-activated cystathionine β-synthase/H2S signaling drives drug resistance in acute myeloid leukemia through CD36-mediated fatty acid metabolism.","authors":"Qianpeng Li, Qin Li, Haifeng Han, Maowen Liu, Nannan Lyu, Zhiyuan Qiu, Rui Zhang, Xiaofeng Li, Xuehong Ran","doi":"10.1093/jleuko/qiaf065","DOIUrl":"10.1093/jleuko/qiaf065","url":null,"abstract":"<p><p>Hypoxia-associated hydrogen sulfide (H2S) accumulation promotes chemotherapy resistance in solid tumor cells. This study delved into the mechanism by which cystathionine β-synthase (CBS)/H2S signaling is involved in the development of acute myeloid leukemia (AML) resistance to cytarabine (ara-C) under hypoxic conditions. The levels of CBS and H2S in AML cells and ara-C-resistant AML cells were evaluated. Subsequently, the expression of CBS and H2S under normoxic and hypoxic conditions in ara-C-resistant AML cells was further scrutinized. sh-CBS or sh-thrombospondin 1 (THBS1) was transfected into ara-C-resistant AML cells, which were then exposed to 1% oxygen and/or ara-C. The cell viability, apoptosis, and lipid metabolism level were evaluated by the cell counting kit-8, flow cytometry, kit, and qPCR. Simultaneously, the methylation of THBS1 was detected via methylation-specific PCR analysis. The expression of CBS and H2S is elevated in ara-C-resistant AML cells, rising proportionally with diminishing oxygen concentration. In ara-C-resistant AML cells, hypoxia stimulated cell viability, suppressed apoptosis, augmented total cholesterol and triacylglycerol levels, upregulated the levels of CD36 and carnitine palmitoyltransferase-1α, as well as downregulated short-chain acyl-CoA dehydrogenase and peroxisome proliferator-activated receptor α levels, while these effects of hypoxia were all reversed by sh-CBS. sh-CBS notably decreases the hypermethylation level of THBS1 in ara-C-resistant AML cells. sh-THBS1 reversed the regulatory effect of sh-CBS on lipid metabolism, cell viability, and apoptosis in ara-C-resistant AML cells. Conversely, sh-CD36 effectively overrode the reversal impact of sh-THBS1. Activation of CBS/H2S signaling in a hypoxic environment participates in the ara-C resistance of AML cells by facilitating CD36-mediated fatty acid metabolism through the mediation of THBS1 methylation.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144078571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From killers to hoplites: neutrophils in skin barrier defense.","authors":"Austin Lowery, Yanfang Peipei Zhu, Catherine C Hedrick","doi":"10.1093/jleuko/qiaf074","DOIUrl":"10.1093/jleuko/qiaf074","url":null,"abstract":"<p><p>Neutrophils are traditionally known as short-lived pathogen-killing cells, but recent work published in Nature by Hidalgo and colleagues uncovers a novel role for neutrophils in maintaining skin integrity. Using transcriptomics, imaging, and genetic models, the study reveals that skin-infiltrating neutrophils produce collagen, particularly COL3A1, to regulate tissue mechanics and form matrix-rich \"shields\" that prevent pathogen entry. Collagen production by these specialized neutrophils in the skin was TGFβ-dependent and essential for wound protection, as its disruption led to disorganized skin architecture and increased bacterial invasion. This work redefines neutrophils as dynamic matrix-builders in barrier tissues, offering new insights into immune-tissue crosstalk and advancing our understanding of wound healing and host defense.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202771/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early increased monocyte-to-lymphocyte ratio as a potential biomarker of bacterial sepsis in patients with severe COVID-19.","authors":"Edna Basilio-Gálvez, Ruth Lizzeth Madera-Sandoval, Arturo Cérbulo-Vázquez, Jessica Lakshmi Prieto-Chávez, Graciela Libier Cabrera-Rivera, María Teresa García-de la Rosa, Patricia Esther Miranda-Cruz, Jesús Emmanuel Juárez-Palacios, Joseph García-Rodríguez, Julio Vázquez-Estrada, Virginia Lima-Salinas, Diana Alba-Lugo, Juan Carlos Anda-Garay, Alejandra Yarensy Macías-Gutiérrez, Luis Eduardo Martínez-Ascencio, Alejandra López-Teófilo, Laura Romero-Gutiérrez, Luis Alejandro Sánchez-Hurtado, Diana Ávila-Alberto, Nancy Rivas, Constantino López-Macías, Eduardo Antonio Ferat-Osorio, Lourdes Andrea Arriaga-Pizano","doi":"10.1093/jleuko/qiaf064","DOIUrl":"10.1093/jleuko/qiaf064","url":null,"abstract":"<p><p>Monocytes are pivotal during inflammation. Sepsis added to COVID-19 increases mortality and inflammation. However, the role of monocytes in this condition is unclear. Our aim was to determine monocyte frequencies and HLA-DR expression related to size distribution in patients with severe COVID-19 with or without sepsis. Twenty-nine patients with COVID-19, 9 patients with COVID-19 + sepsis, and 11 non-COVID nonseptic volunteers were recruited. Patients with COVID-19 + sepsis had increased monocyte count (P = 0.004) and monocyte-to-lymphocyte ratio (MLR, P = 0.01) prior to bacterial sepsis development. The monocyte-to-lymphocyte ratio had an area under the curve of 77.8%, suggesting its potential utility in predicting bacterial sepsis up to 21 d before positive culture. In these patients, smaller intermediate and nonclassical monocytes expressed higher levels of HLA-DR (P < 0.05). Diminished HLA-DR expression in bigger monocytes was associated with an increase in severity and inflammatory markers (r2 values equal to or higher than ±0.4, P < 0.05). Our results suggest that the monocyte-to-lymphocyte ratio could be a potential early marker for bacterial sepsis development in patients with severe COVID-19.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"117 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TFEB-mediated proinflammatory response in murine macrophages induced by acute Alpha7 nicotinic receptor activation.","authors":"Havisha H Honwad, Mehran Najibi, Jiali Shen, Savior Watts, Accalia M Fu, Balazs Koscso, Milena Bogunovic, Javier E Irazoqui","doi":"10.1093/jleuko/qiaf077","DOIUrl":"10.1093/jleuko/qiaf077","url":null,"abstract":"<p><p>Transcription factors TFEB and TFE3 are crucial for regulating autophagy, lysosomal biogenesis, and lipid metabolism, and have significant roles in macrophage function and innate immunity. The alpha7 nicotinic acetylcholine receptor (α7nAChR), a ligand-gated Ca2+ channel known for its therapeutic potential in neurological and inflammatory disorders, has been implicated in modulating immune responses by modulating macrophage function. Stimulation of α7nAChR with chemical agonists has been claimed to activate TFEB in pancreatic acinar cells and neurons. However, the impact of α7nAChR activation on TFEB and TFE3 in macrophages remained unknown, posing an important question due to the potential implications for inflammation regulation. This study investigates the effects of acute α7nAChR activation on TFEB-mediated responses in murine macrophages using the specific agonist PNU-282987. We demonstrate that α7nAChR stimulation triggers TFEB nuclear translocation and lysosomal expansion. Surprisingly, PNU-282987 induces a broad proinflammatory gene signature without concomitant cytokine secretion, suggesting an uncoupling of gene expression from cytokine release. Mechanistically, TFEB activation requires the lysosomal Ca2+ exporter MCOLN1 and the Ca2+-dependent phosphatase PPP3/calcineurin. Additionally, PNU-282987 elevates reactive oxygen species (ROS) levels, and ROS are involved in TFEB activation by PNU-282987. Notably, even with α7nAChR deletion, compensatory ROS-mediated TFEB activation persists, suggesting the involvement of additional mechanisms of action for PNU-282987. Our findings reveal a novel α7nAChR-TFEB signaling axis in macrophages, offer new insights into the cholinergic regulation of immune responses, establish a baseline for comparison with disease states, and identify potential therapeutic targets for modulating inflammation.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144174349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha-1 antitrypsin modulates neutrophil phenotype and function: implications for inflammatory regulation.","authors":"Regina Oshins, Ishan Patel, Laith Khartabil, Divya Sai Katikaneni, Yogesh Scindia, Nazli Khodayari","doi":"10.1093/jleuko/qiaf091","DOIUrl":"10.1093/jleuko/qiaf091","url":null,"abstract":"<p><p>Alpha-1 antitrypsin, the most abundant protease inhibitor within the plasma, plays a crucial role in regulating neutrophils' function during inflammation. Alpha-1 antitrypsin deficiency is associated with excessive neutrophilic inflammation, yet the mechanisms underlying alpha-1 antitrypsin's role in neutrophil trafficking remain poorly understood. Here, we demonstrate alpha-1 antitrypsin is essential for maintaining neutrophil polarity, directional migration, and tissue infiltration during inflammation. Using alpha-1 antitrypsin-knockout mice, we found these mice present increased numbers of neutrophils in the bone marrow, impaired mobilization, and reduced liver neutrophil infiltration following lipopolysaccharide-induced systemic inflammation. Flow cytometry and immunohistochemistry revealed alpha-1 antitrypsin-knockout neutrophils had lower CD44 expression and defective F-actin polarization leading to impaired chemotaxis. Importantly, low expression of CD44 prevented efficient adhesion and transmigration of alpha-1 antitrypsin-knockout neutrophils across liver sinusoidal endothelial cells. Furthermore, chemotaxis assays showed alpha-1 antitrypsin-knockout neutrophils in alpha-1 antitrypsin-deficient media displayed random motility and loss of directional migration toward fMLP (N-Formyl-Met-Leu-Phe), suggesting a critical role for alpha-1 antitrypsin in neutrophil trafficking. Additionally, plasma alpha-1 antitrypsin deficiency delayed neutrophils' rate of phagocytosis. Mechanistically, alpha-1 antitrypsin deficiency resulted in excessive ERK1/2 (Extracellular Signal-Regulated Kinase 1/2) activation in alpha-1 antitrypsin-knockout neutrophils, driving an interleukin-10-enriched environment while suppressing expression of CXCL1 (C-X-C Motif Chemokine Ligand 1) and CXCL10 (C-X-C Motif Chemokine Ligand 10), chemokines essential for neutrophil recruitment. Notably, exposure to wild-type plasma with sufficient alpha-1 antitrypsin restored ERK1/2 activation, CD44 expression, and chemokine levels in alpha-1 antitrypsin-knockout neutrophils, confirming the role of circulating alpha-1 antitrypsin in maintaining neutrophil function. These findings highlight alpha-1 antitrypsin as a key regulator of neutrophil trafficking, adhesion, and immune signaling, with implications for alpha-1 antitrypsin deficiency-related inflammatory disorders.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"117 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AML1-ETO and CCND2 overexpression- cooperate to drive acute myeloid leukemia initiation and progression.","authors":"Junli Mou, Qianqian Huang, Xiaoyu Liu, Wenbing Liu, Yu Liu, Yihan Mei, Runxia Gu, Yingxi Xu, Kejing Tang, Zheng Tian, Haiyan Xing, Qing Rao, Min Wang, Shaowei Qiu, Jianxiang Wang","doi":"10.1093/jleuko/qiaf072","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf072","url":null,"abstract":"<p><p>Increasing numbers of clinical cohorts have detected CCND2 mutations in acute myeloid leukemia (AML), especially in the subtype of AML with t(8;21) translocation. As known, this AML subtype is characterized by the formation of AML1-ETO fusion gene. However, AML1-ETO fusion gene alone is not sufficient to drive leukemia development, additional mutations are required for leukemogenesis. In this study, we aim to investigate whether mutated CCND2 can cooperate with AML1-ETO fusion gene to drive leukemia initiation and progression. In our previous study, the conditional AML1-ETO knock-in mouse model (AML1/ETO mouse), which represented a pre-leukemia stage as myeloproliferative neoplasm phenotype, was established. To confirm whether the AML1-ETO and CCND2 mutation can cooperate to drive leukemia, the mice transduction and transplantation model harboring both AML1-ETO and CCND2 gene (both wildtype and mutant) were established. Upon the assessment of the phenotype, biological features and survival of the mice, only the mice overexpressing the AML1-ETO and CCND2 simultaneously were eventually progressed to leukemia. Besides, compared to mice overexpressing AML-ETO gene alone, mTOR and cell cycle-related pathways were significantly enriched in mice harboring both AML1-ETO and CCND2. And the selective mTOR inhibitor, Everolimus, can reduce the leukemia burden and prolong the survival of this group of mice. In conclusion, it was confirmed that introduction of the CCND2 gene into the AML/ETO pre-leukemia mice could trigger the development of leukemia. It was also confirmed that CCND2 overexpression resulted in the upregulation of the mTOR pathway and inhibiting the pathway might be a therapeutic strategy for this subtype of leukemia.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of skin microbial ecology on γδ T-cell immune pathways in allergic dermatitis models in mice.","authors":"Zonghao You, Xiaoyan Zhang, Sujie Huang, Denghui Chen, Yifan Zhu, Gen Li, Xi Chen","doi":"10.1093/jleuko/qiae244","DOIUrl":"10.1093/jleuko/qiae244","url":null,"abstract":"<p><p>Atopic dermatitis is a complex disease influenced by alterations in the skin microbiome and immune dysregulation. Despite the recognized role of these factors, the specific pathways by which distinct microbial populations affect skin immunity remain insufficiently understood. On a molecular level, the pathogenesis of atopic dermatitis involves critical cytokines such as IL-4, IL-17, interferon-γ, and IL-10, which contribute to the imbalance in T helper cell responses. Importantly, gamma-delta (γδ) T cells, which produce these cytokines and infiltrate affected epithelial cells in atopic dermatitis, have been underexplored. This study seeks to alleviate atopic dermatitis symptoms in mice by adjusting both peripheral and local immune environments through the transplantation of skin microbiota. By employing 16S rRNA sequencing, we characterized the skin microbiome of the mouse model. Our results demonstrate that microbiota intervention significantly reduces skin thickening and serum IgE levels in DNCB-induced atopic dermatitis mice. Additionally, changes in skin microbiota modulated immune cell dynamics, restoring the T helper 1 / T helper 2 balance and leading to clinical improvement. These findings highlight the critical role of skin microbiota in shaping immune responses, positioning microbiota-based therapies as a potential treatment for atopic dermatitis.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142581401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}