Journal of immunology最新文献_第10页

Identification of novel protein biomarkers of macrophage polarization using comparative proteomic analyses of murine primary macrophages. 利用小鼠原代巨噬细胞的比较蛋白质组学分析鉴定巨噬细胞极化的新蛋白生物标志物。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-18 DOI: 10.1093/jimmun/vkaf202

Baolong Liu, Phuong Linh Nguyen, Pengfei Li, Michael J Naldrett, Sophie Alvarez, Jiujiu Yu

{"title":"Identification of novel protein biomarkers of macrophage polarization using comparative proteomic analyses of murine primary macrophages.","authors":"Baolong Liu, Phuong Linh Nguyen, Pengfei Li, Michael J Naldrett, Sophie Alvarez, Jiujiu Yu","doi":"10.1093/jimmun/vkaf202","DOIUrl":"10.1093/jimmun/vkaf202","url":null,"abstract":"Macrophages comprise the first line of host responses against injury and pathogens and therefore are critically engaged in tissue repair, host defense, and homeostasis maintenance. Depending on the surrounding microenvironment, macrophages polarize into a wide spectrum of immunophenotypes with 2 extreme opposite ends-proinflammatory M1 and anti-inflammatory M2. Elucidating the biochemical bases of distinct macrophage immunophenotypes, as well as discriminating between these phenotypes, are paramount to understanding the contributions of macrophage subpopulations to health and diseases. In this study, murine bone marrow-derived macrophages were treated with LPS or IL-4 to induce the M1/M(LPS) or M2/M(IL-4) state, respectively. Comparative proteomic analyses demonstrate that M1 and M2 macrophages have their own unique protein landscapes. The signature proteins of M1 and M2 macrophages are engaged in distinct signaling pathways, which offer the biochemical bases for their specialized functions. The plasma membrane proteins Clec4e and Cd72 are identified as new biomarkers to discriminate murine M1 and M2 macrophages, respectively. Comparison of the proteomes of murine and human macrophages leads to identification of 2 new shared M1 biomarkers, Gbp2/GBP2 and Acod1/ACOD1. In addition, CLEC4E is validated as a new M1 biomarker for human primary macrophages. This study provides an unbiased protein dataset of murine primary M1/M(LPS) and M2/M(IL-4) macrophages for future research in macrophage biology. The plasma membrane localization of the new biomarkers Clec4e and Cd72 facilitates their labeling and detection. The new M1 biomarkers shared by human and mouse primary macrophages have potential broad applications in both basic research and clinical practice.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873538","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}

引用次数: 0

Premature thymic involution in young Foxn1lacz mutant mice causes peripheral T cell phenotypes similar to aging-induced immunosenescence. 年幼的Foxn1lacz突变小鼠胸腺过早退化导致外周T细胞表型类似于衰老诱导的免疫衰老。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-18 DOI: 10.1093/jimmun/vkaf193

Shiyun Xiao, Seung Woo Kang, Kimberly E Oliva, Wen Zhang, Kimberly D Klonowski, Nancy R Manley

{"title":"Premature thymic involution in young Foxn1lacz mutant mice causes peripheral T cell phenotypes similar to aging-induced immunosenescence.","authors":"Shiyun Xiao, Seung Woo Kang, Kimberly E Oliva, Wen Zhang, Kimberly D Klonowski, Nancy R Manley","doi":"10.1093/jimmun/vkaf193","DOIUrl":"10.1093/jimmun/vkaf193","url":null,"abstract":"The thymus is a primary lymphoid organ generating self-restricted and self-tolerant naïve T cells. Early in life the thymus starts to involute, resulting in decreased naïve T cell output which may be more self-reactive, leading to an increased prevalence of autoimmunity. A decrease in the transcription factor FOXN1 is an early event in thymic involution. Using the Foxn1lacz model, we studied how premature thymic involution affects the thymic microenvironment, thymocytes, and peripheral T cell immunity. We found that early thymic involution led to aged-like thymic epithelial cells that resulted in aged-like thymocyte phenotypes, with a significant decrease in CD4+ single-positive T cells. We also observed severe lymphopenia in Foxn1lacz mice caused by the premature decrease in T cell production, resulting in a peripheral T cell phenotype similar to de novo aged peripheral T cells. Moreover, following T cell receptor stimulation, Foxn1lacz peripheral T cells had reduced IL-2 secretion and strong initial IFN-γ responses, resembling aged wild-type peripheral T cell responses. Lastly, influenza response in Foxn1lacz had a reduction in some aspects of T cell responses to influenza infection. Our study shows an independent and direct impact of premature thymic involution on both thymopoiesis and peripheral immune niches likely contributing to immunosenescence and inflammaging as observed in the elderly population.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873539","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}

引用次数: 0

Resolving the field: a role for Nod2 in T cells. 解析该领域：Nod2在T细胞中的作用。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-18 DOI: 10.1093/jimmun/vkaf204

Leah M Huey, Holly L Rosenzweig, Ruth J Napier

引用次数: 0

Brucella abortus induces dynamin-related protein 1 (DRP1)-dependent mitochondrial fission in infected macrophages via stress sensor IRE1α altering metabolic function. 流产布鲁氏菌通过应激传感器IRE1α诱导感染巨噬细胞的动力蛋白相关蛋白1 （DRP1）依赖性线粒体分裂，改变代谢功能。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-14 DOI: 10.1093/jimmun/vkaf198

Erika S Guimarães, Marco Túlio R Gomes, Pedro M Moraes-Vieira, Sergio C Oliveira

{"title":"Brucella abortus induces dynamin-related protein 1 (DRP1)-dependent mitochondrial fission in infected macrophages via stress sensor IRE1α altering metabolic function.","authors":"Erika S Guimarães, Marco Túlio R Gomes, Pedro M Moraes-Vieira, Sergio C Oliveira","doi":"10.1093/jimmun/vkaf198","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf198","url":null,"abstract":"Brucella abortus exploits the endoplasmic reticulum as a site for replication, triggering the unfolded protein response (UPR). While various pathogens have developed strategies to manipulate mitochondrial dynamics, the mechanisms underlying bacterial infection and mitochondrial dynamics interactions remain poorly understood. Here, we demonstrate that B. abortus induces mitochondrial fragmentation via IRE1α. Our findings reveal that Brucella-induced mitochondrial fission is mediated by dynamin-related protein 1 (DRP1), a pivotal regulator of mitochondrial fission. Moreover, we have demonstrated that DRP1 is activated by the UPR. Brucella-induced fragmentation leads to mitochondrial energetic dysfunction, marked by impaired mitochondrial ATP production and compromised bioenergetic capacity. Furthermore, we reveal a novel role for DRP1 in regulating type I IFN production and signaling during B. abortus infection. Mechanistically, mitochondrial fission facilitates the release of mitochondrial DNA, a potent inducer of type I IFN responses. Despite its impact on mitochondrial function and IFN signaling, DRP1 does not influence the control of B. abortus infection. Our findings uncover a unique mechanism by which B. abortus-induced UPR triggers mitochondrial fragmentation affecting innate immune signaling and cellular metabolism.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855493","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}

引用次数: 0

Humanized DRAGA mice are a valuable model to study novel immunotherapies for HIV-1. 人源化DRAGA小鼠是研究HIV-1新免疫疗法的一个有价值的模型。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-13 DOI: 10.1093/jimmun/vkaf185

Pongthorn Pumtang-On, Liliana K Thron, Negin Goodarzi, Brianna C Davey, Emily N Sevcik, Natalie Coleman-Fuller, Ahmad F Karim, Vaiva Vezys, Mangala Rao, Branden S Moriarity, Mary S Pampusch, Aaron K Rendahl, Sofia A Casares, Pamela J Skinner

{"title":"Humanized DRAGA mice are a valuable model to study novel immunotherapies for HIV-1.","authors":"Pongthorn Pumtang-On, Liliana K Thron, Negin Goodarzi, Brianna C Davey, Emily N Sevcik, Natalie Coleman-Fuller, Ahmad F Karim, Vaiva Vezys, Mangala Rao, Branden S Moriarity, Mary S Pampusch, Aaron K Rendahl, Sofia A Casares, Pamela J Skinner","doi":"10.1093/jimmun/vkaf185","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf185","url":null,"abstract":"Humanized (h) DRAGA mice are a promising in vivo model for investigating immunotherapies for treating HIV infections. These mice are not only susceptible to HIV infection, but they also develop functional human immune cells, including T cells and B cells, as well as follicular-like structures that mimic lymphoid B-cell follicles, where HIV-producing cells concentrate during infection in a manner similar to that found in humans. This study evaluated HIV-infected hDRAGA mice as a model for testing the safety, tissue targeting, and efficacy of HIV-specific CAR/CXCR5 T cells. We also evaluated whether HIV infection in hDRAGA mice can be suppressed by antiretroviral therapy. We produced functional HIV-specific CAR/CXCR5 T cells from disaggregated hDRAGA splenocytes and infused cell products into HIV-infected hDRAGA mice. CAR/CXCR5 T cells persisted in hDRAGA mice for the duration of the study, peaking 6 d postinfusion. Treatment with CAR/CXCR5 T cells appeared to be safe, with 100% survival rate and no noticeable changes in pathology. Six days after infusion, CAR/CXCR5 T cells had accumulated in the follicle-like structures in the spleen, with many in direct contact with HIV-producing cells. However, CAR/CXCR5 T-cell treatment did not reduce viral loads compared to controls, likely because CD4 T cells in the infused product became infected with and spread HIV infection. Despite this, all mice treated with antiretroviral therapy showed complete suppression of viral replication, indicating that HIV infection was treatment responsive in the DRAGA mice. These studies indicate that hDRAGA mice are a valuable model to study cellular immunotherapies for HIV.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847122","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}

引用次数: 0

Regulation of B-cell development and differentiation by microRNAs during immune response and their implications in immunological disorders. 免疫应答过程中microrna对b细胞发育和分化的调控及其在免疫紊乱中的意义。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-13 DOI: 10.1093/jimmun/vkaf203

Urbi Roy, Sathees C Raghavan

引用次数: 0

Roxadustat enhances inflammation and metabolic reprogramming in human leukocytes by affecting oxygen sensing. 罗沙司他通过影响氧感应增强人白细胞的炎症和代谢重编程。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-12 DOI: 10.1093/jimmun/vkaf167

Anna Wrobeln, Tina Martin Schäper, Yves Schild, Lars Kleine-Möllhoff, Tristan Leu, Johannes Jägers, Bettina Budeus, Alexandra Heinrich, Hannah Schwarzer-Sperber, Roland Schwarzer, Verena Börger, Sandra Winning, Joachim Fandrey

{"title":"Roxadustat enhances inflammation and metabolic reprogramming in human leukocytes by affecting oxygen sensing.","authors":"Anna Wrobeln, Tina Martin Schäper, Yves Schild, Lars Kleine-Möllhoff, Tristan Leu, Johannes Jägers, Bettina Budeus, Alexandra Heinrich, Hannah Schwarzer-Sperber, Roland Schwarzer, Verena Börger, Sandra Winning, Joachim Fandrey","doi":"10.1093/jimmun/vkaf167","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf167","url":null,"abstract":"Since its approval in 2019, hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitors, like roxadustat, have been used for treatment of anemia in chronic kidney disease. However, the impact of HIF stabilization on circulating leukocytes remains largely unexplored. In this study, we examined how clinically relevant concentrations of roxadustat affect human PBMCs. We evaluated the effects of roxadustat on leukocyte viability, HIF pathway activation via protein and gene expression analysis, metabolic shifts through oxygen consumption and extracellular acidification, and immune subpopulation dynamics and activation through single-cell RNA sequencing. We also explored the effects of roxadustat combined with lipopolysaccharide to simulate conditions of inflammatory hypoxia. Roxadustat did not compromise PBMC viability, but triggered HIF-1α protein accumulation, glycolytic reprogramming, and cytokine gene expression. Single-cell RNA sequencing revealed shifts in leukocyte subpopulations, and a combined treatment with lipopolysaccharide showed an enhanced inflammatory response. We found roxadustat to be a modulator of immune activity, revealing its potential to activate specific leukocyte subpopulations and amplify inflammatory responses. Our study sheds new light on the immunological dimensions of HIF stabilization and its implications for patient care, urging further exploration of its therapeutic and safety profile.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835234","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}

引用次数: 0

Activation and exhaustion of CD8 T cells in patients with chronic lymphocytic leukemia treated with ibrutinib and pembrolizumab. 依鲁替尼和派姆单抗治疗慢性淋巴细胞白血病患者的CD8 T细胞激活和衰竭

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-12 DOI: 10.1093/jimmun/vkaf182

Rui Mu, Katherine M Hornick, Neelam Redekar, Jonathan Chen, Pia Nierman, Susan Soto, Rohan Herur, Clare Sun, Layla Saleh, Maissa Mhibik, Keyvan Keyvanfar, Inhye E Ahn, Adrian Wiestner

{"title":"Activation and exhaustion of CD8 T cells in patients with chronic lymphocytic leukemia treated with ibrutinib and pembrolizumab.","authors":"Rui Mu, Katherine M Hornick, Neelam Redekar, Jonathan Chen, Pia Nierman, Susan Soto, Rohan Herur, Clare Sun, Layla Saleh, Maissa Mhibik, Keyvan Keyvanfar, Inhye E Ahn, Adrian Wiestner","doi":"10.1093/jimmun/vkaf182","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf182","url":null,"abstract":"Immune checkpoint blockade has been shown to restore anti-tumor T-cell function and elicit durable responses in select solid and hematopoietic malignancies. However, single-agent anti-programmed death 1 (PD-1) antibodies proved less efficacious in patients with chronic lymphocytic leukemia (CLL). In patients with high-risk or relapsed/refractory CLL, we conducted a phase 2 study testing the combination of lead-in ibrutinib and up to 2 cycles of fludarabine, followed by continuous therapy with ibrutinib and 17 cycles of pembrolizumab administered every 3 weeks. A total of 15 patients were enrolled. In 10 patients evaluable for response, we observed 1 complete response and 9 partial responses. There was no discernible benefit of the combination beyond what is expected from ibrutinib monotherapy. However, 3 weeks after the first dose of pembrolizumab, we detected CD8 T-cell proliferation in a subset of patients, whom we called \"immune responders.\" In the responders, CD27-expressing CD8 T cells were relatively increased over immune nonresponders. Paired single-cell RNA and TCR sequencing revealed clonal expansion of activated GZMK+ CD8 effector memory and terminally differentiated effector cells. After 6 months of pembrolizumab treatment, the proportion of activated and proliferating CD8 T cells returned to baseline levels. Similarly, most novel clonotypes identified after 1 cycle of pembrolizumab decreased in frequency on long-term treatment. In summary, pembrolizumab did not improve the clinical response over ibrutinib monotherapy but transiently activated distinct clonotypes of CD8 T cells in a subset of CLL patients.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835273","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}

引用次数: 0

Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection. 直接在nod中基因消融Bcl3可完全保护1型糖尿病。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-12 DOI: 10.1093/jimmun/vkaf189

Jeremy J Racine, Jennifer R Dwyer, Harold D Chapman, Amy Bell, Raymond F Robledo, David V Serreze

{"title":"Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.","authors":"Jeremy J Racine, Jennifer R Dwyer, Harold D Chapman, Amy Bell, Raymond F Robledo, David V Serreze","doi":"10.1093/jimmun/vkaf189","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf189","url":null,"abstract":"It was previously reported that genetic ablation of the NF-κB atypical inhibitor Bcl3 through congenic introduction of a 129P2-embryo derived knockout allele (Bcl3tm1Ver) accelerated autoimmune diabetes in the NOD mouse model. Conversely, we found that direct CRISPR-mediated ablation of this gene in the NOD/ShiLtDvs substrain completely inhibited diabetes development. Our CRISPR approach excised exons 3-7 within the NOD Bcl3 gene. These new NOD-Bcl3-/- mice had very low levels of insulitis, indicating protective mechanisms elicited early in the disease process. Dissimilar to reports of Bcl3 ablation in nonautoimmune C57BL/6-background mice, we found that splenic and lymph node B cells were not reduced. However, splenic T2 and MZ cells were increased with a disruption of B-cell follicle formation. Diabetes protection was associated with elevated splenic and lymph node regulatory T cells, and increases in CD4 effector and CD8 central memory T cells in pancreatic lymph nodes. Diabetes protection was overridden by anti-PD-1 administration. Previous studies suggested that Bcl3 may influence diabetes development downstream of Nfkbid, another atypical NF-κB inhibitor. Indeed, co-introduction of this Bcl3 knockout allele also completely blocked diabetes in NOD-Nfkbid-/- mice normally characterized by accelerated disease. Collectively these findings support the possibility that prior findings may have been driven by congenic introduction of linked modifier genes from non-NOD background strains and initiate a critical reevaluation of the role of Bcl3 in type 1 diabetes pathogenesis.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835226","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}

引用次数: 0

CXCL1 augments host defense against Legionella pneumophila through the IL-18-IFN-γ axis and neutrophil homeostasis. CXCL1通过IL-18-IFN-γ轴和中性粒细胞稳态增强宿主对嗜肺军团菌的防御。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-08 DOI: 10.1093/jimmun/vkaf191

Ky V Hoang, John Le, Xiaoqian Shan, Samithamby Jeyaseelan

{"title":"CXCL1 augments host defense against Legionella pneumophila through the IL-18-IFN-γ axis and neutrophil homeostasis.","authors":"Ky V Hoang, John Le, Xiaoqian Shan, Samithamby Jeyaseelan","doi":"10.1093/jimmun/vkaf191","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf191","url":null,"abstract":"Legionella pneumophila causes severe pneumonia, resulting in acute lung injury. L. pneumophila pneumonia induces neutrophil recruitment to the lung through CXC chemokines. Previously, blocking CXCR2, the common receptor for CXC chemokines, but not CXCL1 or CXCL2, resulted in attenuated neutrophil accumulation and reduced survival following pulmonary L. pneumophila infection. However, gene-deficient mice were unavailable at that time and therefore, mechanisms of host protection and neutrophil homeostasis, including granulopoiesis and neutrophil release from the bone marrow, have not been investigated. Here, we delineated the role of CXCL1 and CXCL2 in host defense and neutrophil homeostasis using gene-deficient mice. Deficiency of CXCL1, but not CXCL2, impairs bacterial clearance and neutrophil accumulation in the lung. Furthermore, the increase of IL-18 and IFN-γ proteins in the lung caused by L. pneumophila infection is decreased in Cxcl1-/- mice. Moreover, this reduction in IFN-γ production in Cxcl1-/- mice is associated with a decrease in the γδTCR-expressing IFN-γ+ subset. In vivo treatment with IL-18 or IFN-γ was found to restore neutrophil-dependent bacterial clearance in Cxcl1-/- mice. Production of CXCL1 not only by hematopoietic cells, but also by nonhematopoietic cells, is critical to augment host defense. In Cxcl1-/- mice, there is an impairment in emergency granulopoiesis in bone marrow and in neutrophil release to the blood. Also, Il-18-/- mice displayed impairment of neutrophil recruitment to the lung and bacterial clearance, neutrophil release, and emergency granulopoiesis. Collectively, CXCL1 derived from both hematopoietic and nonhematopoietic cells is essential to control L. pneumophila infection through the IL-18-IFN-γ axis and neutrophil homeostasis.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835275","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}

引用次数: 0