Journal of Leukocyte Biology最新文献

{"title":"Relevance of mouse and human IBD patient-derived colon organoids to investigate intestinal macrophage differentiation.","authors":"Maxime Costa, Muriel Pottier, Marie Jacob, Pauline Zarnitzky, Benjamin Segain, Martin Figeac, Shéhérazade Sebda, Frédéric Leprêtre, Bertrand Meresse, Julie Demaret, Benoit Foligné, Annie Standaert, Benjamin Bertin","doi":"10.1093/jleuko/qiaf004","DOIUrl":"10.1093/jleuko/qiaf004","url":null,"abstract":"<p><p>The gastrointestinal tract is a remarkable example of complex biology, with a constant dialogue between the intestinal epithelium, in close contact with the microbiota, and the immune cells that protect the gut from infection. Organoids have revolutionized our approach to modeling the intestinal cellular compartment and have opened new avenues for unraveling the mechanisms involved in intestinal homeostasis and chronic pathogenesis, such as inflammatory bowel disease. To date, few models have been established to explore the role of the colon, which is, however, the main site of inflammation in ulcerative colitis. Here, we used conditioned media produced by colon organoids from mice or humans (control patients and patients with ulcerative colitis) to investigate the relationship between macrophages and the colon epithelium. We addressed transcriptomic profiles of organoid conditioned media-stimulated bone marrow-derived macrophages and found that these cells exhibited a unique anti-inflammatory signature distinct from that of conventional in vitro IL-4/IL-13 M2-differentiated macrophages. In addition, organoid conditioned media induced a clear CD5 antigen-like-mediated immunoregulatory effect characterized by a significant reduction in lipopolysaccharide-induced inducible nitric oxide synthase expression. In line, organoid conditioned media from human colons inhibited lipopolysaccharide-dependent inflammatory cytokine expression in human monocyte-derived macrophages. Interestingly, the inflammatory marker CD68 was reduced by organoid conditioned media from control patients but not from patients with ulcerative colitis, suggesting epithelial dysfunction in patients with ulcerative colitis. Our results report new regulatory mechanisms in the colon and highlight the importance of developing new in vitro models to better characterize the relationship between the intestinal epithelium and immune mucosal cells.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006761","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":"Insights into the emerging immune checkpoint NR2F6 in cancer immunity.","authors":"Hayat Miftah, Hamza Benthami, Abdallah Badou","doi":"10.1093/jleuko/qiae260","DOIUrl":"10.1093/jleuko/qiae260","url":null,"abstract":"<p><p>NR2F6 has emerged as a key player in immune regulation, especially in cancer immunity. It has been reported that NR2F6 could suppress the antitumor immune response and has therefore been suggested as a possible target in cancer immunotherapy. In this review, we start by describing the complex structure of the NR2F6 gene and its multifaceted biological functions. Then, we examine its expression in distinct immune cells and cancer cells, elucidating its role in cancer progression. Subsequently, we highlight the predictive significance of NR2F6 for cancer patient outcomes, suggesting its possible use as a prognostic biomarker. Finally, we discuss the emerging potential of NR2F6 as a therapeutic target, presenting novel opportunities for developing effective cancer immunotherapy strategies.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142895297","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 role of CD57+γδ T cells in the immune pathogenesis of patients with sepsis.","authors":"Liman Li, Nenggang Jiang, Yongmei Jin, Chuan Yang, Yang Fu","doi":"10.1093/jleuko/qiaf015","DOIUrl":"10.1093/jleuko/qiaf015","url":null,"abstract":"<p><p>The immune responses are dysregulated during sepsis. This study aimed to investigate the role of CD57+γδ T cells in the immune pathogenesis of patients with sepsis. We characterized the transcriptomic profile of peripheral γδ T cells from patients with sepsis using smart RNA sequencing. Additionally, we assessed the ratios and immune functional signatures of CD57+γδ T cells in sepsis through flow cytometry. The cytotoxic capacity of the CD57+γδ T-cell subset was also validated in vitro. Our findings revealed a reduction in the proportion of peripheral CD57+γδ T cells in patients with sepsis, which was correlated with clinical outcomes. Compared with CD57-γδ T cells, CD57+γδ T cells exhibited a markedly altered immunophenotype, including decreased expression of costimulatory molecules and increased expression of proinflammatory factors and cytotoxic granules. Our study proposed a potential role of CD57 in sepsis and its utility as a novel biomarker for patients with sepsis.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399205","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":"Extended repertoire of CXC chemokines acting as agonists and antagonists of the human and murine atypical chemokine receptor ACKR2.","authors":"Rafael Luís, Brian F Volkman, Martyna Szpakowska, Andy Chevigné","doi":"10.1093/jleuko/qiaf013","DOIUrl":"10.1093/jleuko/qiaf013","url":null,"abstract":"<p><p>Atypical chemokine receptors are a subfamily of important regulators of chemokine functions. Among them, ACKR2 has long been considered a scavenger of multiple inflammatory chemokines exclusively from the CC family. Recently, we demonstrated the ability of ACKR2 to scavenge the CXC chemokine CXCL10, previously reported to bind solely the classical receptor CXCR3. This discovery emphasized the need for systematic reassessments of chemokine-receptor pairings. In this work, we established a highly sensitive NanoBRET-based competition binding assay using a novel proprietary ACKR2 modulator (LIH222) and applied it in a comprehensive reassessment of the pairings between human and murine chemokines and their respective ACKR2 orthologs. We confirmed CXCL10 as a ligand for the human but also the mouse ACKR2. We also identified CXCL5, CXCL11, and CXCL12 as new CXC chemokines for both ACKR2 orthologs. Furthermore, we showed that CXCL2 is a ligand for the human but not the mouse ACKR2, whereas CXCL1 binds the mouse but not the human receptor. Finally, we found that N-terminally truncated CXCL5 (CXCL58-78) loses its capacity to bind ACKR2, whereas the removal of the first 2 residues of CXCL11 (CXCL113-73) enhances its antagonist potency, showing a tendency toward a reduction of the receptor basal interactions with β-arrestins. Altogether, this study demonstrates that ACKR2 is not exclusive to CC chemokines, and although with a weaker affinity, it can also bind and scavenge a subset of inflammatory and homeostatic CXC chemokines important for the regulation of the immune system.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12017343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188772","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":"Regulation and therapeutic potential of NLRP3 inflammasome in intestinal diseases.","authors":"Wenxue Li, Tianya Liu, Yaoxing Chen, Yan Sun, Chengzhong Li, Yulan Dong","doi":"10.1093/jleuko/qiaf014","DOIUrl":"https://doi.org/10.1093/jleuko/qiaf014","url":null,"abstract":"<p><p>The NOD-like receptor family, particularly the protein 3 that contains the pyrin domain (NLRP3), is an intracellular sensing protein complex responsible for detecting patterns associated with pathogens and injuries. NLRP3 plays a crucial role in the innate immune response. Currently, a wide range of research has indicated the crucial importance of NLRP3 in various inflammatory conditions. Similarly, the NLRP3 inflammasome plays a significant role in preserving intestinal balance and impacting the advancement of diseases. In addition, several randomized trials have demonstrated the safety and efficacy of targeting NLRP3 in the treatment of colitis, colorectal cancer, and related diseases. This review explores the mechanisms of NLRP3 assembly and activation in the gut. We describe its pathological significance in intestinal diseases. Finally, we summarize current and future therapeutic approaches targeting NLRP3 for intestinal diseases.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":"117 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039813","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":"Gut-resident regulatory T cells (GTregs) play a pivotal role in maintaining bone health under postmenopausal osteoporotic conditions.","authors":"Asha Bhardwaj, Leena Sapra, Divya Madan, Vineet Ahuja, Hanuman Prasad Sharma, Thirumurthy Velpandian, Pradyumna Kumar Mishra, Rupesh K Srivastava","doi":"10.1093/jleuko/qiaf008","DOIUrl":"10.1093/jleuko/qiaf008","url":null,"abstract":"<p><p>Osteoporosis is a skeletal condition characterized by the deterioration of bone tissue. The immune system plays a crucial role in maintaining bone homeostasis and combating the development of osteoporosis. Immunoporosis is the term used to describe the recent convergence of research on the immune system's role in osteoporosis. The gut harbors the largest component of the immune system, and there is growing evidence that intestinal immunity plays a vital role in regulating bone health. Gut-resident regulatory T cells are essential in inhibiting immune responses and preventing various inflammatory manifestations. Our findings show that gut-resident regulatory T cells are pivotal in the pathophysiology of postmenopausal osteoporosis. We investigated the potential of gut-resident regulatory T cells in regulating the development of bone cells in vitro. We observed that gut-resident regulatory T cells significantly enhance osteoblastogenesis with concomitant inhibition of osteoclastogenesis in a cell ratio-dependent manner. We further report that the deficiency of short-chain fatty acids in osteoporotic conditions substantially disrupts the composition of gut-resident regulatory T cells, leading to a loss of peripherally derived regulatory T cells and an expansion of thymus-derived regulatory T cells. Moreover, the administration of probiotics Lactobacillus rhamnosus (UBLR-58) and Bifidobacterium longum (UBBL-64) modulated the gut-resident regulatory T cells compartment in a short-chain fatty acid-dependent manner to mitigate inflammatory bone loss in postmenopausal osteoporosis. Notably, short-chain fatty acid-primed gut-resident regulatory T cells were found to be significantly more effective in inhibiting osteoclastogenesis compared with unprimed gut-resident regulatory T cells. Altogether our results, for the first time, highlight the crucial role of gut-resident regulatory T cells in the pathophysiology of postmenopausal osteoporosis, with potential clinical implications.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006674","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":"Noncanonical NF-κB signaling in dendritic cells is required for ATP-driven indoleamine 2,3-dioxygenase 1 induction through P2Y11 receptor.","authors":"Darina Ocadlikova, Benedetta Fiordi, Sara Trabanelli, Valentina Salvestrini, Marilena Ciciarello, Dorian Forte, Emma Campazzi, Letizia Vitali, Serenella C Cipollitta, Anna Pegoraro, Camilla Jandus, Francesco Di Virgilio, Elena Adinolfi, Michele Cavo, Antonio Curti","doi":"10.1093/jleuko/qiaf010","DOIUrl":"10.1093/jleuko/qiaf010","url":null,"abstract":"<p><p>Extracellular ATP released from dying cells, including tumor cells, is a key mediator of inflammation and tolerance by binding to purinergic receptors on dendritic cells (DCs), resulting in inflammasome activation (via P2X7R), DC maturation (via P2Y11R), and indoleamine-2,3-dioxygenase 1 upregulation. However, the regulation of ATP-driven Indoleamine-2,3-dioxygenase 1 expression in human DCs has been poorly investigated. In this work, we aimed to investigate the ATP-driven molecular regulation of indoleamine-2,3-dioxygenase 1 expression via purinergic receptors and to provide an in-depth characterization of ATP-driven T regulatory cells induced by indoleamine-2,3-dioxygenase 1-expressing DCs. We identified P2Y11R as being responsible for ATP-driven indoleamine-2,3-dioxygenase 1 upregulation, and noncanonical NF-kB as a molecular pathway associated with ATP-dependent indoleamine-2,3-dioxygenase 1 induction through P2Y11R. Then, we investigated-but did not confirm-an involvement of inflammasome machinery through P2X7R in indoleamine-2,3-dioxygenase 1 upregulation. Finally, we evaluated the role of ATP catabolism via ATP ectonucleotidases, i.e. CD39 and CD73 and its main product adenosine, in regulating the generation of indoleamine-2,3-dioxygenase 1-driven T regulatory cells. We found that ATP-driven indoleamine-2,3-dioxygenase 1 upregulation is associated with CD73 upregulation and adenosine production. Additionally, ATP-treated indoleamine-2,3-dioxygenase 1-positive mature DCs induce PD-1-expressing bona fide suppressive T regulatory cells via adenosine A2AR. Collectively, a more in-depth understanding of ATP-driven immune-regulatory mechanisms through indoleamine-2,3-dioxygenase 1 regulation in human DCs leading to the induction of T regulatory cells can have clinical implications for the development of indoleamine-2,3-dioxygenase 1 inhibitors in cancer patients, especially in combination with immunotherapy such as an anti-CD73 or adenosine receptor agonist and immunogenic chemotherapy.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143122730","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":"Pregnancy is associated with a simultaneous but independent increase in circulating CD177pos and immature low-density granulocytes.","authors":"Agnes Dahlstrand Rudin, Agnes Torell, Jordan Popovic, Marit Stockfelt, Bo Jacobsson, Anna Rudin, Karin Christenson, Anna-Carin Lundell, Johan Bylund","doi":"10.1093/jleuko/qiae255","DOIUrl":"10.1093/jleuko/qiae255","url":null,"abstract":"<p><p>The neutrophil marker CD177 (NB1, HNA-2a) is expressed by 0-100% of circulating neutrophils in any given donor, dividing neutrophils into 2 distinct subpopulations (CD177pos and CD177neg). High proportions of CD177pos blood neutrophils have been linked to both systemic infections and a range of inflammatory pathologies, but whether this is a cause or a consequence of disease is not known. Many conditions displaying elevated CD177pos neutrophil proportions are also accompanied by the presence of circulating low-density granulocytes. Accordingly, it is tempting to speculate that these 2 events are connected (i.e. that proportions of CD177pos neutrophils increase as a result of an enlarged pool of circulating low-density granulocytes). A temporary increase in CD177pos neutrophils, in combination with the presence of low-density granulocytes, has been reported during pregnancy. The present study aimed to investigate whether elevated proportions of CD177pos neutrophils in peripheral blood from pregnant women can be attributed to the presence of low-density granulocytes. We found that low-density granulocytes were indeed present in pregnancy and included both immature and activated mature neutrophils. The proportion of CD177pos low-density granulocytes increased over time during pregnancy and correlated with a simultaneous increase in immature cells. However, most immature neutrophils were CD177neg, meaning that increased release of immature cells cannot explain the increased proportions of the CD177pos subtype. Therefore, although low-density granulocytes and CD177pos neutrophils are expanded simultaneously during pregnancy, these events occur independently from each other.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854455","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":"Suppression of NF-κB/NLRP3 by nanoligomer therapy mitigates ethanol and advanced age-related neuroinflammation.","authors":"Paige E Anton, Shannon Twardy, Prashant Nagpal, Julie A Moreno, Matthew A Burchill, Anushree Chatterjee, Nicolas Busquet, Michael Mesches, Elizabeth J Kovacs, Rebecca L McCullough","doi":"10.1093/jleuko/qiaf024","DOIUrl":"10.1093/jleuko/qiaf024","url":null,"abstract":"<p><p>Binge alcohol use is increasing among aged adults (>65 yr). Alcohol-related toxicity in aged adults is associated with neurodegeneration; yet, the molecular underpinnings of this age-related sensitivity to alcohol are not well described. Studies utilizing rodent models of neurodegenerative disease reveal heightened activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Nod-like receptor 3 (NLRP3) mediate microglia activation and associated neuronal injury. Our group, and others, have implicated hippocampal-resident microglia as key producers of inflammatory mediators; yet, the link between inflammation and neurodegeneration has not been established in models of binge ethanol exposure and advanced age. Here, we report binge ethanol increased the proportion of NLRP3+ microglia in the hippocampus of aged (18 to 20 mo) female C57BL/6N mice compared with young (3 to 4 mo). In primary microglia, ethanol-induced expression of reactivity markers and NLRP3 inflammasome activation were more pronounced in microglia from aged mice compared with young. Using a NLRP3-specific inhibitor (OLT1177) and a novel brain-penetrant Nanoligomer that inhibits NF-κB and NLRP3 translation (SB_NI_112), we find ethanol-induced microglial reactivity can be attenuated by OLT1177 and SB_NI_112 in microglia from aged mice. In a model of intermittent binge ethanol exposure, SB_NI_112 prevented ethanol-mediated microglia reactivity, IL-1β production, and tau hyperphosphorylation in the hippocampus of aged mice. These data suggest early indicators of neurodegeneration occurring with advanced age and binge ethanol exposure are driven by NF-κB and NLRP3. Further investigation is warranted to explore the use of targeted immunosuppression via Nanoligomers to attenuate neuroinflammation after alcohol consumption in the aging populations.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12022636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557152","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":"Prolonging neutrophil room-temperature storage with clinically approved solutions: implications for granulocyte transfusion.","authors":"Marie-Michèle Labrecque, Marie-Ève Allard, Andréa Murru, Guillaume Paré, Jason P Acker, Sylvie Lesage, Mélissa Girard, Maria J Fernandes","doi":"10.1093/jleuko/qiae258","DOIUrl":"10.1093/jleuko/qiae258","url":null,"abstract":"<p><p>Granulocyte concentrates (GCs) are leukocyte preparations enriched in neutrophils that can potentially save neutropenic patients from life-threatening, antimicrobial-resistant infections. The main challenge of GC transfusions is preserving the viability and antimicrobial activity of neutrophils beyond 24 h to reduce the logistical burden on collection centers and increase the availability of this cell therapy. Thus, the aim of this study was to explore extending the ex vivo viability and antimicrobial activity of GC neutrophils up to 72 h with a unique combination of the clinically approved additives Plasma-Lyte (PL), SAGM, AS-3, and Alburex. Neutrophils isolated from healthy donors were resuspended in autologous plasma at the same concentration as in GCs, diluted with various combinations of PL, SAGM, AS-3, and/or Alburex with or without the addition of buffers, and stored at room temperature for up to 72 h. During storage, neutrophil viability, phagocytosis, and intracellular reactive oxygen species production were measured by flow cytometry. Extracellular reactive oxygen species production was measured by spectrophotometry and chemotaxis by the number of calcein-stained neutrophils that migrated toward the chemotactic peptide, N-formyl-Met-Leu-Phe (fMLF). The same assays were performed on pooled, residual leukocyte units generated by the Reveos system, after storage in the additive combination that most effectively preserved the viability and function of isolated neutrophils. The additive combination that best performed in the majority of the assays contained PL, buffers, and AS-3. Neutrophil viability was preserved for a maximum of 48 h and phagocytosis of opsonized bacteria and reactive oxygen species production up to 72 h of storage at room temperature. In contrast, fMLF-induced chemotaxis decreased by 20% after 24-h storage while extracellular reactive oxygen species production increased significantly within the same time period. Supplementing GCs prepared from pooled, residual leukocyte units with this storage solution after the standard 16- to 24-h processing period as per the blood center guidelines, did not significantly improve the preservation of neutrophil viability and function. Our findings provide proof of concept that mixtures of clinically approved additives can be tailored to significantly prolong the viability and function of freshly isolated neutrophils during room-temperature storage. The unique additive composition of this storage solution that we developed for freshly isolated neutrophils requires further optimization for use with pooled, residual leukocyte units as well as the timepoint at which the solution is added during processing to prolong the viability and functions of neutrophils in this blood product.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882457","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}