Journal of Leukocyte Biology最新文献

{"title":"A narrative review of the mitochondrial DNA-stimulated inflammatory axis in sepsis-induced acute lung injury: cellular mechanisms and therapeutic targeting.","authors":"Shuqi Ma, Qiusha Pan, Ruifeng Zeng, Quanle Liu, Suyi Yang, Jingnan Lin, Shiyi Liu, Ye Ye, Rui Chen, Jun Li","doi":"10.1093/jleuko/qiag077","DOIUrl":"10.1093/jleuko/qiag077","url":null,"abstract":"<p><p>Sepsis-induced acute lung injury (SALI) represents a life-threatening condition with complex pathophysiology. Emerging evidence highlights the mitochondrial DNA (mtDNA)-stimulated inflammatory axis as a pivotal mechanism driving pulmonary inflammation. This narrative review elucidates how mtDNA, released upon cellular damage, acts as a potent damage-associated molecular pattern that activates the cyclic guanosine monophosphate-adenosine monophosphate(cGAMP) synthase-stimulator of interferon genes (STING) pathway. We detail the cell type-specific roles of this axis: In macrophages, it promotes M1 polarization and pyroptosis; in neutrophils, it facilitates neutrophil extracellular trap formation; in lymphocytes, it contributes to T-cell exhaustion; and in structural cells (endothelial and alveolar epithelial cells, fibroblasts), it induces barrier dysfunction, PANoptosis, and fibrotic remodeling. Furthermore, we discuss promising therapeutic strategies that target this axis, including STING inhibitors, mtDNA-neutralizing nanoparticles, and natural compounds, which have shown efficacy in preclinical models. Translating these findings into clinical practice requires future research focused on cell-specific modulation and innovative delivery systems to mitigate the devastating effects of SALI.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217416","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":"Eosinophil Essentials: Identification and Assessment of Activity.","authors":"Sarah Almas, Paige Lacy","doi":"10.1093/jleuko/qiag091","DOIUrl":"https://doi.org/10.1093/jleuko/qiag091","url":null,"abstract":"<p><p>Eosinophils are highly granulated white blood cells first identified as \"granule blood cells\" in the 19th century. In this review, we discuss techniques used to identify these unique cells and explore how they release a range of pro- and anti-inflammatory mediators. They are easily detected with a range of cellular dyes due to highly cationic proteins stored within their crystalloid granules. Cationic proteins include major basic protein (MBP), eosinophil peroxidase (EPX), eosinophil-derived neurotoxin (EDN), eosinophil cationic protein (ECP), and Charcot-Leyden crystal protein (CLC, also known as galectin-10) that serve as potent antimicrobial factors and possess a high affinity for negatively charged molecules including eosin and fluorescein isothiocyanate (FITC). Crystalloid granules are responsible for autofluorescence and nonspecific binding to both fluorophores and antibodies during immunolabeling for fluorescence microscopy, flow cytometry, CyTOF, and other antibody-based detection methods. Eosinophils release a plethora of mediators that have roles in immunity and homeostasis. Here, we describe six different categories of mediators released by eosinophils and their analyses: (1) cationic granule proteins (MBP, EPX, EDN, ECP, and CLC), (2) cytokines and chemokines, (3) reactive oxygen species, (4) eicosanoid production, (5) eosinophil extracellular trap formation, and (6) exosomes. We also describe novel transcriptional markers where new subtypes of eosinophils are characterized through the development of single cell RNA sequencing, showing additional transcripts appearing in eosinophils from patients with diseases. Future work on eosinophils is anticipated to lead to a greater understanding of their role in immunity and diseases based on novel emerging techniques.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352153","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":"Neutrophils in Tumorigenesis and Progression: Dual Roles and Clinical Translation.","authors":"Kexin Hu, Hongyu Li, Puwei Huang, Xiyue Zhang, Rong Hu, Qianming Du","doi":"10.1093/jleuko/qiag079","DOIUrl":"https://doi.org/10.1093/jleuko/qiag079","url":null,"abstract":"<p><p>Neutrophils, the most abundant innate immune cells, act as first responders in host defense via phagocytosis, degranulation, ROS production and Neutrophil Extracellular Traps (NETs) formation. Emerging evidence reveals that neutrophils are highly plastic and heterogeneous, acting as critical regulators in tumor biology. Tumor-derived CXCL8 and G-CSF drive emergency granulopoiesis, neutrophil recruitment and functional reprogramming, leading to immune suppression, angiogenesis, matrix remodeling, metastasis and therapy resistance. In specific contexts, neutrophils also exert anti-tumor effects by direct cytotoxicity, enhancing T-cell responses and restricting metastasis, displaying a dual role in cancer. Notably, anti-tumor neutrophils are rare in steady-state tumors but emerge during therapy-induced immune remodeling. Single-cell and spatial multi-omics have challenged the classical N1/N2 dichotomy. Tumor-associated neutrophils (TANs) and polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) are now viewed as overlapping, dynamic populations along a functional continuum, shaped by maturation, metabolism, hypoxia and tissue niches. This review summarizes the dual roles of neutrophils in tumor progression, abnormal granulopoiesis, functional polarization, and revised concepts of TANs and PMN-MDSCs. We highlight NETosis, immune suppression, metabolic reprogramming and therapy resistance, and outline clinical translation including biomarkers (e.g., NLR) and therapeutic strategies. Current challenges and future directions are discussed, aiming to precisely target pro-tumor neutrophils while preserving host antimicrobial immunity.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148258327","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":"Tissue adaptation of eosinophils.","authors":"Clotilde Marie Lacroix, Kalyani Kulkarni, Nicola Laura Diny","doi":"10.1093/jleuko/qiag064","DOIUrl":"10.1093/jleuko/qiag064","url":null,"abstract":"<p><p>Eosinophils are increasingly recognized as tissue-resident immune cells that take on diverse functions. Recent studies have shed light on the pathways that result in tissue-specific eosinophil phenotypes. In this review, we discuss the process of tissue adaptation covering the local environmental cues that trigger adaptation, the transcriptional reprograming that occurs in response, and the phenotypic, metabolic, and functional adaptation that leads to varied eosinophil populations across the body. We further examine the relative impact of trained immunity and systemic factors versus local signals on eosinophil plasticity in the context of homeostasis and inflammation.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147963978","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":"Distinct lymphocyte immune signatures to nivolumab and recombinant IL-7 ex vivo in patients with sepsis.","authors":"Timothy Arthur Chandos Snow, Walter Pisciotta, Gladys Martir, Caroline Copeland, Athanasios Sekeris, Abhishek Das, Mervyn Singer, David Brealey, Nishkantha Arulkumaran","doi":"10.1093/jleuko/qiag057","DOIUrl":"https://doi.org/10.1093/jleuko/qiag057","url":null,"abstract":"<p><p>Therapeutic modulation of sepsis-induced immune dysfunction by targeting lymphocyte dysfunction with recombinant IL-7 (rIL-7) and anti-PD-1 (e.g. nivolumab) has shown promise in preclinical and early clinical studies. Prior to conducting large randomized controlled trials, an in-depth understanding of the changes induced by rIL-7 or nivolumab (and their differences) in patients with sepsis is imperative. We performed a prospective observational cohort study including patients admitted to the intensive care unit with sepsis and characterized their T lymphocyte phenotype using flow cytometry. The ability of T lymphocytes to respond to a stimulus (using anti-CD3/CD28 beads) and the effect of rIL-7 or nivolumab on T lymphocyte immunophenotype ex vivo was assessed. In a cohort of 55 patients, CD4+ and CD8+ T lymphocyte PD-1 was higher and IL-7R lower compared with healthy volunteers. In a subset of 24 intensive care unit patients in whom in-depth immunophenotype was characterized, ex vivo response of lymphocytes to anti-CD3/CD28 beads was reduced compared with healthy volunteers, simultaneously inducing features consistent with immune activation and immunosuppression. rIL-7 was associated with a greater spectrum of changes compared with nivolumab. The response to rIL-7 and nivolumab was influenced by anti-CD3/CD28 bead costimulation. rIL-7 and nivolumab elicited distinct T lymphocyte responses ex vivo, and the changes were influenced by T lymphocyte activation. It needs to be determined if similar changes occur in vivo, which may influence the choice of immunomodulatory therapy in sepsis.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"118 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148352171","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":"Immune cell landscape reveals 5 immune-related subtypes and molecular characteristics with prognostic and therapeutic implications in pan-cancer.","authors":"Hongjiu Wang, Na Wang, Siyu He, Xiaoling Wen, Feifan Xiong, Denghui Guo, Jie Shen, Sirui Li, Jiangying Liang, Xinyao Huang, Ziyang Yi, Pengyuan Zhai, Xiao Ling Gao, Zhenzhen Wang, Xia Li","doi":"10.1093/jleuko/qiag062","DOIUrl":"10.1093/jleuko/qiag062","url":null,"abstract":"<p><p>The immunotherapy represents the most promising new cancer treatment approach but due to the high heterogeneity of the tumor microenvironment among patients, only a small portion of patients respond to a certain immunotherapy. Therefore, identifying the immune-related subtypes and immune molecular characteristics is of great guiding significance for improving the response and results of immunotherapy and personalized treatment of cancer. This study aims to identify immune subtypes across various cancers based on immune cell infiltration profiles and assess their clinical significance. We analyzed immune cell infiltration data from The Cancer Genome Atlas (TCGA) using Tumor IMmune Estimation Resource (TIMER), Microenvironment Cell Populations-counter (MCP), and Estimate the Proportion of Immune and Cancer cells (EPIC) algorithms to ensure consistency. Clustering analysis categorized 9,648 tumor samples into 5 immune subtypes (I to V) based on their infiltration profiles. We evaluated the relationship between these subtypes and patient survival, tumor characteristics, and genetic mutations. Five distinct immune subtypes were identified as cold tumors with low immune infiltration and hot tumors with high immune infiltration. Survival analysis revealed significant differences, with hot tumors associated with better prognosis except subtype IV. Mutational analysis identified isocitrate dehydrogenase 1 (IDH1) mutations as a significant prognostic biomarker for cold tumors, accounting for 85.3% of mutations in this subtype. We also identified 35 differentially expressed genes, leading to the construction of classifiers with high accuracy for predicting treatment responses. These findings highlight the heterogeneity of immune cell infiltration in tumors and its impact on patient prognosis and treatment sensitivity. The findings suggest that immune subtypes can serve as valuable biomarkers, particularly IDH1 mutations in cold tumors, paving the way for personalized cancer therapies.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"118 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345539","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":"Streptococcus anginosus activates the NLRP3 inflammasome to promote inflammatory responses from macrophages.","authors":"Anika M Arias, Dakota M Reinartz, Chloe Sairs, Sangeetha Senthil Kumar, Harrison C Byrnes, Justin E Wilson","doi":"10.1093/jleuko/qiag061","DOIUrl":"10.1093/jleuko/qiag061","url":null,"abstract":"<p><p>Chronic inflammation and oral dysbiosis are common features of oral squamous cell carcinoma (OSCC). The commensal bacterium Streptococcus anginosus is increased in oral diseases, including OSCC. Our previous work revealed that S. anginosus promotes inflammatory responses from macrophage cell lines; however, the molecular mechanism by which S. anginosus interacts with macrophages to instigate this response remains to be investigated. Here, we found S. anginosus activated primary bone marrow-derived macrophages (BMMs), which presented increased NF-κB activation and downstream inflammatory cytokines TNF-α, IL-6, and IL-1β at 24 h after infection. S. anginosus viability, TLR2, TLR4, and MyD88 were dispensable for NF-κB activation, but each promoted the induction of distinct downstream inflammatory mediators, with only MyD88 being necessary for NF-κB activation in response to heat-killed S. anginosus. S. anginosus replicated intracellularly within BMMs without causing cell death and induced expression of inflammasome sensors AIM2, NLRC4, and NLRP3. S. anginosus-infected BMMs lacking the inflammasome adapter protein ASC (Asc-/-) or caspase-1 (Caspase1-/-) had significantly diminished IL-1β production compared with wild-type (WT) BMMs, indicating that S. anginosus activated the inflammasome. S. anginosus primarily triggered the inflammasome through NLRP3: S. anginosus-infected Nlrp3-/- BMMs and NLRP3 inhibitor (MCC950)-treated WT BMMs displayed diminished IL-1β production compared with WT controls. Lastly, S. anginosus-infected Asc-/-, and to a lesser extent Nlrp3-/-, mice displayed reduced weight loss, reduced inflammatory cytokines, and increased bacterial burden compared with C57BL/6 mice. These findings indicate S. anginosus replicates within macrophages and promotes a proinflammatory response in part through activating the NLRP3 inflammasome.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839043","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":"Homozygous kinase-dead Csf1r mutation in outbred mice reveals essential and redundant functions of tissue resident macrophages.","authors":"Sebastien Jacquelin, Emma Maxwell, Isis Taylor, Emma Green, Conan J O O'Brien, Eline E Jessen, Ginell Ranpura, Jintao Guo, Fathima Nooru-Mohamed, Yajun Liu, Sahar Keshvari, Stephen Huang, Emily Cooper, Steven W Lane, Cameron Flegg, Maria A Kasherman, Kamil Sokolowski, Allison R Pettit, David A Hume, Katharine M Irvine","doi":"10.1093/jleuko/qiag074","DOIUrl":"10.1093/jleuko/qiag074","url":null,"abstract":"<p><p>The proliferation, differentiation, and survival of cells of the macrophage lineage depends on signals from the macrophage colony-stimulating factor receptor (CSF1R). On a C57BL/6J background homozygous kinase-dead Csf1r mutation (Csf1rE631K/E631K-E631Km/m) causes perinatal lethality. By contrast, E631Km/m mice on a mixed genetic background (C57 × BALB/c) were osteoclast-deficient/osteopetrotic and growth retarded but did not develop hydrocephalus or other major structural brain abnormalities seen in inbred Csf1r-/- mice, and they were viable as adults. Outbred E631Km/m mice lacked tissue-resident macrophages detected with a Csf1r-EGFP transgene or F4/80 in most major organs, including the brain, but aside from reproductive organs, which were underdeveloped, no gross histological abnormalities were observed. E631Km/m genotype was associated with reduced blood monocytes, the loss of circulating C1Q, reduced IGF1, and increased CSF1. In mice, F4/80+/CD169+ resident marrow macrophages are believed to be essential components of erythroblastic and hematopoietic island niches. These cells were undetectable in E631Km/m marrow. Their absence was associated with granulocytosis and B-cell deficiency in marrow, blood, and spleen, whereas the relative abundance of pluripotent and committed progenitors was not affected. Erythropoietic homeostasis was also maintained; erythroblasts were physically associated with a minor residual population of CSF1R-independent CD169-/F4/80+ marrow macrophages. We conclude that many developmental and homeostatic functions attributed to mouse resident-tissue macrophages are redundant, species-specific, or restricted to inbred strains.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211456","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":"Glucocorticoid-driven gene expression in circulating monocytes and neutrophils in health and severe inflammation.","authors":"Arthur Molendijk, Leo Koenderman","doi":"10.1093/jleuko/qiag068","DOIUrl":"10.1093/jleuko/qiag068","url":null,"abstract":"<p><p>Glucocorticoids (GCs) are used as anti-inflammatory and immunosuppressive drugs in many immune mediated diseases, but their use in sepsis and shock is controversial. This is caused in part by a lack of information regarding the responding cell types and GC-regulated genes in vivo. We used large collections of public blood transcriptomic datasets and different GC-induced query genes to obtain 2 robust gene expression correlation signatures of GC induction, either in the absence or in the presence of severe inflammation. GC signature 1 originated from circadian cortisol with biases for gene expression in natural killer cells and neutrophils. GC signature 2 originated from GC in severe inflammation, mainly with biases for gene expression in monocytes and neutrophils. Many genes upregulated by GC treatment in septic shock and burn shock were also present as high-ranking genes in GC signatures, which pointed to their direct regulation by GC. Robust GC signatures were also obtained from dataset collections of different tissues for comparison, and of monocytes and neutrophils, separately. Gene induction by GC was put into a wider framework of gene expression in circulating monocytes and neutrophils in health and during systemic inflammation, which included macrophage-like cells and a hypoxia-related gene expression signature in monocytes in severe inflammation. We present and interpret a large number of GC-regulated genes in different blood cells and tissues in vivo and select 2 whole blood transcriptomic biomarker gene sets, GC-1 and GC-2, for monitoring cortisol action in health and in severe inflammation, respectively.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163464","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":"Carboxylesterase 1 contributes to the human macrophage alternative activation response to Th2 cytokine interleukin-4.","authors":"Matthew K Ross, Abdolsamad Borazjani, Hannah L Thrash, Oluwabori Adekanye, J Allen Crow","doi":"10.1093/jleuko/qiag073","DOIUrl":"10.1093/jleuko/qiag073","url":null,"abstract":"<p><p>Carboxylesterase 1 (CES1) is a hydrolytic enzyme with roles in xenobiotic and lipid metabolism. Our previous studies suggested a novel role for CES1 in the regulation of macrophage gene expression following exposure to inflammatory molecules. The nuclear receptor PPARγ has an important role in the M(IL-4) polarization response. Here, we investigated CES1 in human primary macrophages and THP-1 macrophages during M(IL-4) polarization. We hypothesized that ablating CES1's activity would decrease ligand signaling through PPARγ, thereby reducing the M2 polarization response. Inhibition of CES1's activity by small-molecule inhibitors (WWL113 or WWL229) attenuated the mRNA expression of several IL-4-induced M2 markers, including ALOX15. Similar results were found in macrophages in which CES1 or PPARg expression was silenced. Immunoblot and mass spectrometric analyses indicated that IL-4-induced ALOX15 and its enzymatic product, 15-hydroxyeicosatetraenoic acid, were both reduced by CES1 inhibition. Further, a PPARγ antagonist (GW9662) also altered the profile of IL-4-induced M2 markers. The M(IL-4)-induced increase in endogenous PPARγ ligands was augmented by WWL113. Surprisingly, PPARγ agonist \"add-back\" strengthened the WWL113-mediated repression of IL-4-induced ALOX15 expression, whereas IL-4-induced FABP4 mRNA levels were augmented. Collectively, these results suggest that CES1 has a complex role in driving the alternative activation phenotype in response to IL-4, possibly through an ability to influence PPARγ. These findings are consistent with previous work in which CES1 appeared to hold in check the inflammatory response of innate immune cells. The significance of our findings is that CES1 appears to contribute to the integration of extracellular signals that shape macrophage phenotypes.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211396","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}