American Journal of Pathology最新文献_第6页

Intestinal Dysbacteriosis Contributes to Persistent Cognitive Impairment after Resolution of Acute Liver Failure 肠道菌群失调是急性肝衰竭缓解后认知功能持续受损的原因之一。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-13 DOI: 10.1016/j.ajpath.2024.07.014

Zhen Li , Tianning Sun , Zhigang He , Zhixiao Li , Jun Xiong , Hongbing Xiang

{"title":"Intestinal Dysbacteriosis Contributes to Persistent Cognitive Impairment after Resolution of Acute Liver Failure","authors":"Zhen Li , Tianning Sun , Zhigang He , Zhixiao Li , Jun Xiong , Hongbing Xiang","doi":"10.1016/j.ajpath.2024.07.014","DOIUrl":"10.1016/j.ajpath.2024.07.014","url":null,"abstract":"<div><div>Regulating the gut microbiota alleviates hepatic encephalopathy (HE). Whether it is imperative to withhold treatment for microbial imbalance after liver functional recovery remains unclear. The aim of this work was to elucidate the alterations in cognitive behavior, liver function, synaptic transmission, and brain metabolites in acute liver failure (ALF) mice before and after hepatic function recovery. Towards this end, thioacetamide was injected intraperitoneally to establish an ALF mouse model, which induced HE. Hierarchical clustering analysis indicated that while the liver functions normalized, cognitive dysfunction and intestinal dysbacteriosis occurred in the ALF mice 14 days after thioacetamide injection. In addition, fecal microbiota transplantation from the ALF mice with liver function recovery induced liver injury and cognitive impairment. Alterations in synaptic transmission were found in the ALF mice with liver function improvement, and the correlations between the gut bacteria and synaptic transmission in the cortex were significant. Finally, apparent alterations in the brain metabolic profiles of the ALF mice were detected after liver function improvement by performing <sup>1</sup>H nuclear magnetic resonance spectroscopy, suggesting a risk of HE. These results showed that intestinal dysbacteriosis in ALF mice with liver function recovery is sufficient to induce liver injury and cognitive impairment. This indicates that continuous care may be necessary for monitoring microbial imbalance even in patients with ALF-induced HE whose liver function has recovered significantly.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"194 11","pages":"Pages 2076-2090"},"PeriodicalIF":4.7,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential Abundance of DNA Damage Sensors and Innate Immune Signaling Proteins in Inositol Polyphosphate 4-Phosphatase Type II–Negative Triple-Negative Breast Cancer Classified by Immunotype 按免疫类型分类的 INPP4B 阴性 TNBC 中 DNA 损伤传感器和先天免疫信号蛋白的丰度差异。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-13 DOI: 10.1016/j.ajpath.2024.07.015

F. Scott Heinemann , Paul D. Gershon

{"title":"Differential Abundance of DNA Damage Sensors and Innate Immune Signaling Proteins in Inositol Polyphosphate 4-Phosphatase Type II–Negative Triple-Negative Breast Cancer Classified by Immunotype","authors":"F. Scott Heinemann , Paul D. Gershon","doi":"10.1016/j.ajpath.2024.07.015","DOIUrl":"10.1016/j.ajpath.2024.07.015","url":null,"abstract":"<div><div>The influence of neoplastic cells on the tumor microenvironment is poorly understood. In this study, eight patient samples representing two immunotypes of triple-negative breast cancer (TNBC), defined by quantitative histologic criteria as T-cell desert and T-cell infiltrated (TCI), were compared via label-free quantitative protein mass spectrometry of material extracted directly from targeted regions of formalin-fixed, paraffin-embedded tissue sections. Of 2934 proteins quantitated, 439 were significantly differentially abundant, among which 361 were overabundant in TCI-TNBC. The 361-protein group included proteins involved in major histocompatibility complex-I antigen processing and presentation, viral defense, DNA damage response, and innate immune signaling. Immunohistochemical validation of selected proteins showed good positive correlation between neoplastic cell histoscores and label-free quantitation. Extension of immunohistochemical analysis to a total of 58 inositol polyphosphate 4-phosphatase type II–negative TNBC confirmed elevated levels of the DNA damage sensor interferon-γ–inducible protein 16, inflammasome adaptor apoptosis-associated speck-like protein containing a CARD (ASC), and pore-forming protein gasdermin D in TCI-TNBC neoplastic cells. By contrast, cGMP-AMP synthase inhibitor barrier to autointegration factor (BAF) was elevated in the neoplastic cells of T-cell desert TNBC. These findings demonstrate a previously unknown correlation between the degree of T-cell infiltration in inositol polyphosphate 4-phosphatase type II–negative TNBC and the levels, in cognate neoplastic cells, of proteins that modulate innate immune signaling in response to DNA damage.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"194 11","pages":"Pages 2212-2232"},"PeriodicalIF":4.7,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Growth Differentiation Factor 11 Evokes Lung Injury, Inflammation, and Fibrosis in Mice through the Activin A Receptor Type II-Like Kinase, 53kDa–Smad2/3 Signaling Pathway GDF11 通过 ALK5-Smad2/3 信号通路诱发小鼠肺损伤、炎症和纤维化。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-13 DOI: 10.1016/j.ajpath.2024.07.016

Qian Li, Hanchao Li, Li Zhu, Lijuan Zhang, Xiaoyan Zheng, Zhiming Hao

{"title":"Growth Differentiation Factor 11 Evokes Lung Injury, Inflammation, and Fibrosis in Mice through the Activin A Receptor Type II-Like Kinase, 53kDa–Smad2/3 Signaling Pathway","authors":"Qian Li, Hanchao Li, Li Zhu, Lijuan Zhang, Xiaoyan Zheng, Zhiming Hao","doi":"10.1016/j.ajpath.2024.07.016","DOIUrl":"10.1016/j.ajpath.2024.07.016","url":null,"abstract":"<div><div>Growth differentiation factor 11 (GDF11) belongs to the transforming growth factor beta superfamily and participates in various pathophysiological processes. Initially, GDF11 was suggested to act as a rejuvenator by improving age-related phenotypes of the heart, brain, and skeletal muscle in aged mice. Recent studies demonstrate that GDF11 also serves as an adverse risk factor for human frailty and diseases. However, the role of GDF11 in pulmonary fibrosis (PF) remains unclear. This study explored the role and signaling mechanisms of GDF11 in PF. GDF11 expression was markedly up-regulated in fibrotic lung tissues of both humans and mice. Intratracheal administration of commercial recombinant GDF11 caused lung injury, inflammation, and fibrogenesis in mice. Furthermore, adenovirus-mediated secretory expression of mature GDF11 was exacerbated, whereas full-length GDF11 or the GDF11 propeptide (GDF11<sub>1-298</sub>) alleviated bleomycin-induced PF in mice. In <em>in vitro</em> experiments, GDF11 suppressed the growth of alveolar and bronchial epithelial cells (A549 and BEAS-2B) and human pulmonary microvascular endothelial cells, promoted fibroblast activation, and induced epithelial/endothelial-mesenchymal transition. These effects corresponded to the phosphorylation of Smad2/3, and blocking activin A receptor type II-like kinase, 53kDa (ALK5)-Smad2/3 signaling abolished the <em>in vivo</em> and <em>in vitro</em> effects of GDF11. In conclusion, these findings provide evidence that GDF11 acts as a potent injurious, proinflammatory, and profibrotic factor in the lungs via the ALK5-Smad2/3 pathway.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"194 11","pages":"Pages 2036-2058"},"PeriodicalIF":4.7,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Impact of Generative Artificial Intelligence on the External Review of Scientific Manuscripts and Editorial Peer Review Processes 生成式人工智能对科学手稿外部评审和编辑同行评审流程的影响。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-10 DOI: 10.1016/j.ajpath.2024.08.002

Chhavi Chauhan , George Currie

引用次数: 0

Professional Master of Health Science in Laboratory Medicine 检验医学专业硕士；在研究密集型大学的综合课程中培养临床检验科学家。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-10 DOI: 10.1016/j.ajpath.2024.07.013

Avrum I. Gotlieb , Fang-I Lu , William Tsui , Heather Shapiro , Theodore J. Brown , G. Scot Hamilton , Danielle C. Bentley , George M. Yousef , Juan Putra , Rachel Zulla , Rita A. Kandel

{"title":"Professional Master of Health Science in Laboratory Medicine","authors":"Avrum I. Gotlieb , Fang-I Lu , William Tsui , Heather Shapiro , Theodore J. Brown , G. Scot Hamilton , Danielle C. Bentley , George M. Yousef , Juan Putra , Rachel Zulla , Rita A. Kandel","doi":"10.1016/j.ajpath.2024.07.013","DOIUrl":"10.1016/j.ajpath.2024.07.013","url":null,"abstract":"<div><div>A 2-year professional master of health science program at the University of Toronto provides a unique integrated educational program to train allied health science personnel to practice as physician extenders and health care professionals in two high-demand clinical laboratory disciplines, Pathologists' Assistant (PA) and Clinical Embryologist (CE). This report describes an integrated graduate program developed and delivered in a research-intensive laboratory medicine department. The core courses in fundamental biomedical science and in general medical laboratory function and operations formed the foundation on which the requisite clinical skills required to practice as a PA or CE were subsequently delivered as comprehensive CE and PA specialty courses and practicums. Students acquired research skills through courses that teach research methods, critical analysis of research articles, and biostatistics for clinical research scientists. A capstone research project provided students the opportunity to design a research project relevant to the CE or PA fields, perform and analyze the findings, and present the project as an oral abstract and a written scientific article. Students learn to face the clinical challenges by focusing on critical analysis of evidence-based professional practice. The PA field received a 5-year accreditation. CE and PA students presented their clinical research at national and international meetings, with some receiving awards, and published scientific articles. All graduates found meaningful employment in their respective fields, and initial employer response has been favorable.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"194 11","pages":"Pages 2000-2006"},"PeriodicalIF":4.7,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141915851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

This Month in AJP 本月 AJP。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-08 DOI: 10.1016/j.ajpath.2024.08.001

引用次数: 0

Single-Cell Analysis Provides New Insights into the Roles of Tertiary Lymphoid Structures and Immune Cell Infiltration in Kidney Injury and Chronic Kidney Disease. 单细胞分析为了解三级淋巴结构和免疫细胞浸润在肾损伤和慢性肾病中的作用提供了新的视角。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-07 DOI: 10.1016/j.ajpath.2024.07.008

Takahisa Yoshikawa, Motoko Yanagita

{"title":"Single-Cell Analysis Provides New Insights into the Roles of Tertiary Lymphoid Structures and Immune Cell Infiltration in Kidney Injury and Chronic Kidney Disease.","authors":"Takahisa Yoshikawa, Motoko Yanagita","doi":"10.1016/j.ajpath.2024.07.008","DOIUrl":"10.1016/j.ajpath.2024.07.008","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is a global health concern with high morbidity and mortality. Acute kidney injury (AKI) is a pivotal risk factor for the progression of CKD, and the rate of AKI-to-CKD progression increases with aging. Intrarenal inflammation is a fundamental mechanism underlying AKI-to-CKD progression. Tertiary lymphoid structures (TLSs), ectopic lymphoid aggregates formed in nonlymphoid organs, develop in aged injured kidneys, but not in young kidneys, with prolonged inflammation and maladaptive repair, which potentially exacerbates AKI-to-CKD progression in aged individuals. Dysregulated immune responses are involved in the pathogenesis of various kidney diseases, such as IgA nephropathy, lupus nephritis, and diabetic kidney diseases, thereby deteriorating kidney function. TLSs also develop in several kidney diseases, including transplanted kidneys and renal cell carcinoma. However, the precise immunologic mechanisms driving AKI-to-CKD progression and development of these kidney diseases remain unclear, which hinders the development of novel therapeutic approaches. This review aims to describe recent findings from single-cell analysis of cellular heterogeneity and complex interactions among immune and renal parenchymal cells, which potentially contribute to the pathogenesis of AKI-to-CKD progression and other kidney diseases, highlighting the mechanisms of formation and pathogenic roles of TLSs in aged injured kidneys.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blocking IL-17a Signaling Decreases Lung Inflammation and Improves Alveolarization in Experimental Bronchopulmonary Dysplasia 阻断 IL-17a 信号传导可减轻实验性支气管肺发育不良的肺部炎症并改善肺泡化。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-06 DOI: 10.1016/j.ajpath.2024.07.011

Meagan Goates , Amrit Shrestha , Shyam Thapa , Matthew Bettini , Roberto Barrios , Binoy Shivanna

{"title":"Blocking IL-17a Signaling Decreases Lung Inflammation and Improves Alveolarization in Experimental Bronchopulmonary Dysplasia","authors":"Meagan Goates , Amrit Shrestha , Shyam Thapa , Matthew Bettini , Roberto Barrios , Binoy Shivanna","doi":"10.1016/j.ajpath.2024.07.011","DOIUrl":"10.1016/j.ajpath.2024.07.011","url":null,"abstract":"<div><div>Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease of preterm infants that is associated with life-long morbidities. Inflammatory insults contribute to BPD pathogenesis. Although the proinflammatory cytokine, IL-17a, plays a role in various neonatal inflammatory disorders, its role in BPD pathogenesis is unclear. To test the hypothesis that blocking IL-17a signaling decreases lipopolysaccharide (LPS)–mediated experimental BPD in neonatal mice, wild-type mice were injected intraperitoneally with phosphate-buffered saline or LPS during the saccular lung developmental phase. Pulmonary IL-17a expression was determined by enzyme-linked immunosorbent assay and by flow cytometry. LPS-injected mice had higher pulmonary IL-17a protein levels and IL-17a<sup>+</sup> and IL-22<sup>+</sup> cells. γδ T cells, followed by non–T lymphoid cells, were the primary producers of IL-17a. Wild-type mice were then injected intraperitoneally with isotype antibody (Ab) or IL-17a Ab, while they were treated with phosphate-buffered saline or LPS, followed by quantification of lung inflammatory markers, alveolarization, vascularization, cell proliferation, and apoptosis. LPS-mediated alveolar simplification, apoptosis, and cell proliferation inhibition were significantly greater in mice treated with isotype Ab than in those treated with IL-17a Ab. Furthermore, STAT1 activation and IL-6 levels were significantly greater in LPS-exposed mice treated with isotype Ab than in those treated with IL-17a Ab. The study results indicate that blocking IL-17a signaling decreases LPS-mediated experimental BPD.</div></div>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":"194 11","pages":"Pages 2023-2035"},"PeriodicalIF":4.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cancer-Associated Fibroblasts in Intrahepatic Cholangiocarcinoma: Insights into Origins, Heterogeneity, Lymphangiogenesis, and Peritoneal Metastasis. 肝内胆管癌中的癌相关成纤维细胞：对起源、异质性、淋巴管生成和腹膜转移的见解

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-06 DOI: 10.1016/j.ajpath.2024.07.009

Silvia Affὸ, Laura Sererols-Viñas, Gemma Garcia-Vicién, Massimiliano Cadamuro, Sanjukta Chakraborty, Alphonse E Sirica

{"title":"Cancer-Associated Fibroblasts in Intrahepatic Cholangiocarcinoma: Insights into Origins, Heterogeneity, Lymphangiogenesis, and Peritoneal Metastasis.","authors":"Silvia Affὸ, Laura Sererols-Viñas, Gemma Garcia-Vicién, Massimiliano Cadamuro, Sanjukta Chakraborty, Alphonse E Sirica","doi":"10.1016/j.ajpath.2024.07.009","DOIUrl":"10.1016/j.ajpath.2024.07.009","url":null,"abstract":"<p><p>Intrahepatic cholangiocarcinoma (iCCA) denotes a rare, highly malignant, and heterogeneous class of primary liver adenocarcinomas exhibiting phenotypic characteristics of cholangiocyte differentiation. Among the distinctive pathological features of iCCA, one that differentiates the most common macroscopic subtype (eg, mass-forming type) of this hepatic tumor from conventional hepatocellular carcinoma, is a prominent desmoplastic reaction manifested as a dense fibro-collagenous-enriched tumor stroma. Cancer-associated fibroblasts (CAFs) represent the most abundant mesenchymal cell type in the desmoplastic reaction. Although the protumor effects of CAFs in iCCA have been increasingly recognized, more recent cell lineage tracing studies, advanced single-cell RNA sequencing, and expanded biomarker analyses have provided new awareness into their ontogeny, as well as underscored their biological complexity as reflected by the presence of multiple subtypes. In addition, evidence has been described to support CAFs' potential to display cancer-restrictive roles, including immunosuppression. However, CAFs also play important roles in facilitating metastasis, as exemplified by lymph node metastasis and peritoneal carcinomatosis, which are common in iCCA. Herein, the authors provide a timely appraisal of the origins and phenotypic and functional complexity of CAFs in iCCA, together with providing mechanistic insights into lymphangiogenesis and peritoneal metastasis relevant to this lethal human cancer.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Both Classical and Non-Classical Monocytes Patrol Glomerular Capillaries and Promote Acute Glomerular Inflammation. 经典和非经典单核细胞都会巡逻肾小球毛细血管，并促进急性肾小球炎症。

IF 4.7 2区医学

American Journal of Pathology Pub Date : 2024-08-06 DOI: 10.1016/j.ajpath.2024.07.010

ZheHao Tan, Pam Hall, Matthias Mack, Sarah L Snelgrove, A Richard Kitching, Michael J Hickey

{"title":"Both Classical and Non-Classical Monocytes Patrol Glomerular Capillaries and Promote Acute Glomerular Inflammation.","authors":"ZheHao Tan, Pam Hall, Matthias Mack, Sarah L Snelgrove, A Richard Kitching, Michael J Hickey","doi":"10.1016/j.ajpath.2024.07.010","DOIUrl":"10.1016/j.ajpath.2024.07.010","url":null,"abstract":"<p><p>Monocyte patrolling of the vasculature has been ascribed primarily to the non-classical monocyte subset. However, a recent study of the glomerular microvasculature provided evidence that both classical and non-classical monocytes undergo periods of intravascular retention and migration. Despite this, whether these subsets contribute differentially to acute glomerular inflammation is unknown. This study used glomerular multiphoton intravital microscopy to investigate the capacity of classical and non-classical monocytes to patrol the glomerular microvasculature and promote acute, neutrophil-dependent glomerular inflammation. In imaging experiments in monocyte reporter Cx3cr1<sup>gfp/+</sup> mice, co-staining with anti-Ly6B or anti-Ly6C revealed that both non-classical monocytes [CX3C chemokine receptor 1-green fluorescent protein positive (CX3CR1-GFP<sup>+</sup>)] and classical monocytes (CX3CR1-GFP<sup>+</sup> and Ly6B<sup>+</sup> or Ly6C<sup>+</sup>) underwent prolonged (>10 minutes) retention and migration in the glomerular microvasculature. On induction of acute glomerulonephritis, in these behaviors were increased in classical but not non-classical monocytes. Using non-classical monocyte-deficient Csf1r<sup>Cre</sup>Nr4a1<sup>fl/fl</sup> mice, or anti-CCR2 to deplete classical monocytes, the removal of either subset reduced neutrophil retention and activation in acutely inflamed glomeruli, while the depletion of both subsets, via anti-CCR2 treatment in Csf1r<sup>Cre</sup>Nr4a1<sup>fl/fl</sup> mice, led to further reductions in neutrophil activity. In contrast, in a model of CD4<sup>+</sup> T cell-dependent glomerulonephritis, the depletion of either monocyte subset failed to alter neutrophil responses. These findings indicate that both classical and non-classical monocytes patrol the glomerular microvasculature and promote neutrophil responses in acutely inflamed glomeruli.</p>","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0