IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024025680

Rachael C Adams, Kelli P A MacDonald, Geoffrey R Hill

{"title":"The contribution of the monocyte-macrophage lineage to immunotherapy outcomes.","authors":"Rachael C Adams, Kelli P A MacDonald, Geoffrey R Hill","doi":"10.1182/blood.2024025680","DOIUrl":"10.1182/blood.2024025680","url":null,"abstract":"Abstract: Macrophages execute core functions in maintaining tissue homeostasis, in which their extensive plasticity permits a spectrum of functions from tissue remodeling to immune defense. However, perturbations to tissue-resident macrophages during disease, and the subsequent emergence of monocyte-derived macrophages, can hinder tissue recovery and promote further damage through inflammatory and fibrotic programs. Gaining a fundamental understanding of the critical pathways defining pathogenic macrophage populations enables the development of targeted therapeutic approaches to improve disease outcomes. In the setting of chronic graft-versus-host disease (cGVHD), which remains the major complication of allogeneic hematopoietic stem cell transplantation, colony-stimulating factor 1 (CSF1)-dependent donor-derived macrophages have been identified as key pathogenic mediators of fibrotic skin and lung disease. Antibody blockade of the CSF1 receptor (CSF1R) to induce macrophage depletion showed remarkable capacity to prevent fibrosis in preclinical models and has subsequently demonstrated impressive efficacy for improving cGVHD in ongoing clinical trials. Similarly, macrophage depletion approaches are currently under investigation for their potential to augment responses to immune checkpoint inhibition. Moreover, both monocyte and tissue-resident macrophage populations have recently been implicated as mediators of the numerous toxicities associated with chimeric antigen receptor T-cell therapy, further highlighting potential avenues of macrophage-based interventions to improve clinical outcomes. Herein, we examine the current literature on basic macrophage biology and contextualize this in the setting of cellular and immunotherapy. Additionally, we highlight mechanisms by which macrophages can be targeted, largely by interfering with the CSF1/CSF1R signaling axis, for therapeutic benefit in the context of both cellular and immunotherapy.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"1010-1021"},"PeriodicalIF":21.0,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

ALK+ anaplastic large cell lymphoma expressing CD33 and myeloid nuclear differentiation antigen.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027618

Miguel Gonzalez Mancera, Oscar Silva

引用次数: 0

CD7 CAR-T: a bridge to transplant in AML. CD7 CAR-T：通向急性髓细胞白血病移植的桥梁。

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027442

Maksim Mamonkin

引用次数: 0

Over 4 decades, French children teach about LCH.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027160

Barbara A Degar, Barrett J Rollins

引用次数: 0

Air pollution and venous thromboembolism.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027502

Ingrid Pabinger, Cihan Ay

引用次数: 0

Novel mechanisms of resistance in CLL: variant BTK mutations in second-generation and noncovalent BTK inhibitors. CLL耐药的新机制：第二代和非共价BTK抑制剂的变异BTK突变。

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024026672

Constantine S Tam, Shalini Balendran, Piers Blombery

引用次数: 0

Cullin' the herd: Cul5 limits megakaryocyte-biased HSCs.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027680

Eric M Pietras

引用次数: 0

Therapy for MYD88 L265P DLBCL.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027538

Joost S P Vermaat, Ruben A L de Groen

引用次数: 0

Air pollution is associated with increased risk of venous thromboembolism: the Multi-Ethnic Study of Atherosclerosis. 空气污染与静脉血栓栓塞风险增加有关：动脉粥样硬化的多民族研究。

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024026399

Pamela L Lutsey, Jeffrey R Misialek, Michael T Young, Jesse Berman, Claire L Leiser, Zachary C Pope, Mary Cushman, Aaron R Folsom, Joel D Kaufman

{"title":"Air pollution is associated with increased risk of venous thromboembolism: the Multi-Ethnic Study of Atherosclerosis.","authors":"Pamela L Lutsey, Jeffrey R Misialek, Michael T Young, Jesse Berman, Claire L Leiser, Zachary C Pope, Mary Cushman, Aaron R Folsom, Joel D Kaufman","doi":"10.1182/blood.2024026399","DOIUrl":"10.1182/blood.2024026399","url":null,"abstract":"Abstract: Air pollution exposure may induce procoagulant effects, and chronic exposure may be linked to greater risk of venous thromboembolism (VTE). We tested the hypothesis that air pollution is associated with increased VTE risk in the prospective Multi-Ethnic Study of Atherosclerosis, which has well-characterized air pollution measures and information on potential confounding factors. We included 6651 participants recruited in 2000 to 2002 (baseline age range, 45-84 years; 53% female). Air pollution was assessed with a validated spatiotemporal model that incorporates cohort-specific monitoring. Four indexes of air pollution updated each fortnight over follow-up were averaged to estimate participant-level chronic exposure: fine particulate matter ≤2.5 micrometers in aerodynamic diameter (PM2.5), oxides of nitrogen (NOx), nitrogen dioxide (NO2), and ozone (O3). Mean±SD PM2.5 was 13.5±3.0 μg/m3, NO2 17.9±8.2 parts per billion (ppb), NOx 36.1±19.6 ppb, and O3 22.2±3.7 ppb. Incident VTE was identified using hospitalization discharge codes through 2018. A total of 248 VTE events accrued over a median follow-up of 16.7 years. After adjustment for baseline demographics, health behaviors, and body mass index, the hazard ratio (95% confidence interval) for incident VTE associated per 3.6 μg/m3 higher PM2.5 was 1.39 (1.04-1.86); per 13.3 ppb higher NO2 concentration was 2.74 (1.57-4.77); and per 30 ppb higher NOx was 2.21 (1.42-3.44). O3 was not related. In this prospective community-based cohort with individual-level estimation of chronic air pollution exposure, higher average ambient concentrations of PM2.5, NO2, and NOX were associated with greater risk of developing VTE. Findings add to accumulating evidence of adverse health effects attributed to air pollution exposure.","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"1089-1096"},"PeriodicalIF":21.0,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11923424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

AMBRA1 performs a balancing act in β-thalassemia.

IF 21 1区医学

Blood Pub Date : 2025-03-06 DOI: 10.1182/blood.2024027597

Christophe Lechauve, Mitchell J Weiss

引用次数: 0

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