European cytokine network最新文献

{"title":"Co-expression of CCR7 and H3K9me3 identifies aggressive B-cell lymphoma with bone marrow infiltration and poor prognosis.","authors":"Jiawen Chen, Zelin Liu, Keke Huang, Jinlan Li, Yajie Zhang, Dandan Chen, Yanjie Ruan, Ying Pan, Furun An, Yang Wan, Jiyu Wang, Qianshan Tao","doi":"10.32604/ecn.2026.077875","DOIUrl":"https://doi.org/10.32604/ecn.2026.077875","url":null,"abstract":"<p><strong>Objectives: </strong>B-cell lymphoma exhibits significant clinical heterogeneity, necessitating improved biomarkers for risk stratification. C-C chemokine receptor 7 (CCR7) and trimethylation of histone H3 lysine 9 (H3K9me3) are implicated in cellular senescence and tumor invasion. While the clinical significance of their co-expression in lymphomagenesis remains unclear. This study aims to define the expression profiles of CCR7 and H3K9me3 in B-cell lymphoma, explore their correlation with aggressive clinical indicators, and evaluate their combined prognostic value.</p><p><strong>Methods: </strong>The expression of CCR7 and H3K9me3 in tumor tissues from B-cell lymphoma patients was analyzed by immunohistochemical (IHC) double-staining. The mechanistic association between the two was verified by co-immunoprecipitation assays and Western blot (WB) experiments detecting changes in cellular H3K9me3 levels following CCR7 ligand stimulation. The association between co-expression and patient clinical parameters, tumor burden, and progression-free survival (PFS) was evaluated through correlation analysis, Kaplan-Meier survival curves, and Cox regression analysis.</p><p><strong>Results: </strong>H3K9me3 expression was predominantly nuclear, whereas CCR7 was expressed on the cell membrane. Both markers were significantly upregulated in aggressive lymphomas and positively correlated with LDH, β2-microglobulin, and neutrophil percentage. An interaction between CCR7 and H3K9me3 could be demonstrated in that CCR7 ligand stimulation resulted in an upregulation of H3K9me3 expression. Enhanced H3K9me3 expression was associated with bone marrow infiltration. High expression of CCR7 was associated with poorer progression-free survival (PFS), whereas high expression of both CCR7 and H3K9me3 identified patients with the worst prognosis. Univariate and multivariate Cox regression analysis indicated that the combined expression was a potential prognostic biomarker for B-cell lymphoma.</p><p><strong>Conclusion: </strong>Co-elevated CCR7 and H3K9me3 expression defines a high-risk B-cell lymphoma subgroup with high tumor burden, bone marrow infiltration, and poor prognosis, highlighting their potential as biomarkers for risk stratification and candidate therapeutic targeting.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"37 1","pages":"25-39"},"PeriodicalIF":1.2,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Re-evaluating cytokine storm syndromes: dysregulated host defense or contextual immune adaptation?","authors":"Abhishek Vijukumar, Hardik Kumar, Shilpa Debnath, Sourabh Kosey","doi":"10.32604/ecn.2026.078458","DOIUrl":"https://doi.org/10.32604/ecn.2026.078458","url":null,"abstract":"<p><p>Cytokine storm syndromes have become a much-invoked concept to describe severe immunopathology in infectious, inflammatory, and iatrogenic diseases, but the concept is poorly defined and often mechanistically imprecise. High levels of systemic cytokines have often been viewed as indicators of immune dysfunction, and based on this notion, therapeutic interventions focused on general cytokine inhibition are proposed. Nevertheless, a growing number of clinical and experimental data dispute the notion that hypercytokinemia is necessarily pathological. The present paper reconsiders cytokine storm syndromes in the light of an evolutionary, systems-immunology model, and suggests that most cytokine amplification conditions are context-specific host defence programmes, however, not uniform maladaptations of immune regulation. Its major objective is to redefine the cytokine storm syndromes, which are no longer understood as a single, uniformly pathological situation, but as a spectrum of context-specific immune programmes. The paper reviews disease-specific phenotypes of cytokine storms in viral infections, bacterial sepsis, autoimmune diseases, and immune-based therapies, noting considerable variability in cytokine composition, kinetics of production, cytokine-producing cell frequency, and localization in tissues. It also explains how the temporal dynamics, host-specific conditions, and failure of counter-regulatory mechanisms define the difference between cytokine amplification as an adaptation or as a pathological condition. In addition, it considers the clinical consequences of such a refined framework and argues that exploring precision strategies need to consider immune context, disease stage, and signalling thresholds, as opposed to a general use of blocking cytokines. In conclusion, this review attempts to draw a line between adaptive cytokine amplification and maladaptive immunopathology by integrating the insights gained in evolutionary biology and systems immunology.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"37 1","pages":"13-24"},"PeriodicalIF":1.2,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Propolis as a potential modulator of aryl hydrocarbon receptor signaling in inflammation.","authors":"Natália Alvarenga Borges, Larissa Manhães, Ludmilla Dias de Santana E Santana, Jessyca Sousa de Brito, Larissa Fonseca, Ludmila F M F Cardozo, Denise Mafra","doi":"10.32604/ecn.2026.0ECN78096","DOIUrl":"https://doi.org/10.32604/ecn.2026.0ECN78096","url":null,"abstract":"<p><p>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that exhibits antagonistic pleiotropy, mediating both protective and detrimental cellular effects depending on the ligand and context. AhR can be activated by a variety of endogenous and exogenous stimuli, including environmental pollutants, UVB radiation, heme, arachidonic acid metabolites, gut microbiota-derived compounds, and xenobiotics. Upon activation, AhR translocates to the nucleus, where it dimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT) and binds to xenobiotic response elements, inducing the expression of genes involved in xenobiotic metabolism, oxidative stress responses, and inflammatory signaling. In addition to these classical pathways, AhR also modulates immune function by regulating cytokine networks, including IL-17, IL-22, and IL-10, which play key roles in barrier integrity and immune homeostasis. Bioactive dietary compounds, particularly polyphenols such as flavonoids, have emerged as potential modulators of AhR signaling. Propolis, a complex bee-derived product rich in flavonoids and other phenolic compounds, has demonstrated antioxidant and anti-inflammatory effects across multiple experimental models. However, the specific mechanisms through which propolis interacts with AhR signaling remain poorly understood. This mini-review summarizes current evidence on the potential role of propolis as an AhR modulator, discusses its implications for immune regulation, barrier function, and inflammation control, and highlights areas for future research.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"37 1","pages":"1-11"},"PeriodicalIF":1.2,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study of interferon-stimulated gene 15 expression in the medulloblastoma context.","authors":"Eva G Palacios-Serrato, Karen Medina-Abreu, Gabriela Velasco-Loyden, Norma Angélica Lira-Rodríguez, Angeles C Tecalco-Cruz","doi":"10.1684/ecn.2025.0506","DOIUrl":"https://doi.org/10.1684/ecn.2025.0506","url":null,"abstract":"<p><p>Interferon-stimulated gene 15 (ISG15) is a small ubiquitin-like protein that can be conjugated to its target proteins through an enzymatic cascade known as ISGylation, thereby altering their function. Elevated levels of free ISG15 (non-conjugated) and ISGylation are observed in several cancer types, including medulloblastoma (MB) a malignant pediatric cerebellar tumor categorized into four molecular subgroups: Wingless, Sonic Hedgehog, Subgroup 3 (G3), and Subgroup 4 (G4). However, ISG15 gene expression in MB remains unexplored. In this study, we evaluated the ISG15 protein levels, the expression of the ISG15 and ISGylation system, and interferon gamma signaling mediators in human MB samples to propose the role of ISG15 in this tumoral context. ISG15 expression in MB samples was comparatively analyzed against normal tissue using the Oncopression database. Expression levels were further assessed in various pediatric tumors within the Childhood Brain Tumor Tissue Consortium dataset via the University of Alabama at Birmingham Cancer Data Analysis Portal database. ISG15 protein abundance in MB samples was then evaluated via immunohistochemistry on a tumor tissue microarray. To broaden the analysis, ISG15 expression was profiled across multiple MB cell lines using the R2 Genomics Analysis and Visualization Platform. Finally, to determine clinical significance, the association between ISG15 expression and patient survival was assessed using Kaplan-Meier analysis. ISG15 expression was significantly lower in MB samples than in other pediatric tumors (p < 0.05) and normal tissue (p < 0.0001). Immunohistochemical analysis further confirmed a marked reduction in ISG15 protein abundance in MB samples compared to healthy tissue (p < 0.001). Elevated ISG15 levels correlated with improved survival outcomes in the G3 and G4 subgroups (p < 0.05). ISG15 is downregulated in MB tissues compared to controls. High ISG15 expression within the G3/G4 MB subgroups correlates with prolonged survival, suggesting a potential tumor-suppressive function. These results collectively indicate that ISG15 may serve as a valuable prognostic biomarker for G3/G4 MB patients.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 4","pages":"64-73"},"PeriodicalIF":1.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between interleukin-6 promoter polymorphisms and osteoporosis in javanese postmenopausal women.","authors":"Sri Lestari Utami, Mohammad Hidayat, Diana Lyrawati, Loeki Enggar Fitri","doi":"10.1684/ecn.2025.0507","DOIUrl":"https://doi.org/10.1684/ecn.2025.0507","url":null,"abstract":"<p><p>The expression of the interleukin-6 (IL-6) gene promoter and its variations in postmenopausal women of Javanese ethnicity remains unexplored. This study aimed to examine IL-6 promoter polymorphisms at positions -174G/C, -572G/C, -597A/G, and -634C/G and their associations to osteoporosis status in Javanese postmenopausal women. A cross-sectional study was conducted at an elderly integrated service post in Sidoarjo, Indonesia. Among 699 screened individuals, 66 postmenopausal women fulfilled the inclusion and exclusion criteria. Bone mineral density was assessed using dual-energy X-ray absorptiometry (DXA), and osteoporosis status was defined based on T-score values. IL-6 promoter polymorphisms were genotyped by sequencing PCR-amplified promoter regions. IL-6 mRNA expression was assessed using RT-PCR followed by densitometric analysis, and serum IL-6 concentrations were determined using enzyme-linked immunosorbent assay. Our study showed that osteoporosis and osteopenia were predominant (28.8% and 57.6%, respectively), and 13.6% of subjects had normal BMD. The IL-6 promoter variant genotypes and frequencies were as follows: at -174 GG (0.924), CC (0.045), and GC (0.030); at -572 GC (0.424), CC (0.406), and GG (0.167); at -597 GG (0.924) and GA (0.0758) GA (0.076); and at -634 CC (1). The IL-6 mRNA and protein level (median 6.06, IQR 5.0398 pg/mL) were not statistically different among individuals with different genotypes and with normal, osteopenia, or osteoporosis status. Ordinal regression showed that IL-6 promoter polymorphisms were not significantly associated with osteoporosis status. The polymorphisms of the IL-6 promoter were detected in Javanese postmenopausal women; however, such polymorphisms did not correlate with IL-6 mRNA and protein levels nor osteoporosis status. IL-6 promoter polymorphisms were present in Javanese postmenopausal women; however, these variants were not associated with IL-6 expression at the mRNA or protein level, nor with osteoporosis status.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 4","pages":"74-83"},"PeriodicalIF":1.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Igniting the Tumor: Targeting Mitochondrial Stress to Prime Breast Cancer for Immunotherapy.","authors":"Hung-Yu Lin, Hsing-Ju Wu, Pei-Yi Chu","doi":"10.1684/ecn.2025.0504","DOIUrl":"10.1684/ecn.2025.0504","url":null,"abstract":"<p><p>Immunotherapy has demonstrated limited efficacy in immunologically \"cold\" breast cancers characterized by absent T-cell infiltration and inadequate interferon signaling. The purpose of this work is to propose and articulate a mechanistic and therapeutic framework in which mitochondrial stress is deliberately harnessed to convert immunologically \"cold\" breast tumors into \"hot,\" T cell-inflamed, immunotherapy-responsive lesions. This review synthesizes emerging evidence positioning mitochondrial stress as a strategic lever to transform these immune-excluded tumors into inflamed, therapy-responsive lesions. We examine how mitochondrial dysfunction triggers cytosolic release of mitochondrial DNA (mtDNA), a potent damage-associated molecular pattern that activates the cGAS-STING pathway, initiating type I interferon responses and secretion of T-cell-recruiting chemokines such as CCL5 and CXCL10. This axis functions as a \"double-edged sword\"-while acute activation converts \"cold\" tumors into \"hot\" immune-responsive states, chronic engagement drives immunosuppressive cytokine networks and therapeutic resistance, with outcomes varying across breast cancer subtypes. We explore six combination therapeutic strategies: mitochondrial poisons, radiotherapy/chemotherapy, PARP/ATR inhibitors, metabolic reprogramming agents, mitochondrial quality control modulators, and localized mitochondrial stress induction, each paired with immune checkpoint blockade. The review emphasizes \"controlled ignition\" as a paradigm whereby precisely dosed mitochondrial stress amplifies tumor antigenicity and favorable cytokine landscapes while avoiding chronic immunosuppression. Cytokine networks emerge as both integrators and therapeutic targets of mitochondrial-immune crosstalk. Future advances require mapping subtype-specific thresholds, developing tumor-restricted delivery systems, and implementing biomarker-guided trials to safely harness mitochondrial stress, potentially redefining these organelles as programmable immunological adjuvants in breast cancer therapy.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"24-37"},"PeriodicalIF":1.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145997422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of proteases associated with glioblastoma and their modulation by interferon-gamma signaling.","authors":"Enrique Oropeza-Maetínez, Eva G Palacios-Serrato, Marina Macías-Silva, Angeles C Tecalco-Cruz","doi":"10.1684/ecn.2025.0503","DOIUrl":"10.1684/ecn.2025.0503","url":null,"abstract":"<p><p>Glioblastoma is a lethal primary brain tumor that is therapeutically challenging due to its rapid progression. Interferon-gamma (IFN-γ) signaling is altered in glioblastoma. Moreover, proteolytic enzymes, known as proteases, have been linked to the invasive growth of cancerous cells. In this study, we aimed to identify a glioblastoma-associated protease group and to determine its potential connection with IFN-γ signaling. Using cancer expression databases, we analyzed the differential expression of 35 proteases in glioblastoma and healthy brain tissue, and the relevance of their deregulation to patient survival. We also explored correlations between IFN-γ signaling element expression and upregulated proteases in glioblastoma. Additionally, we analyzed the effect of IFN-γ on the levels of these 35 proteases using a protein microarray and found that cathepsin L (CTSL) was upregulated by IFN-γ. Then, we analyzed the modulation of CTSL by IFN-γ in glioblastoma cells using dot blot, western blot, and immunofluorescence assays. We identified 11 proteases (cathepsin B, Z, C, S (CTSB, CTSZ, CTSC, CTSS), matrix metalloproteinase 2, 7, 9 (MMP2, MMP7, MMP9), a disintegrin and metalloproteinase 9 (ADAM9), urokinase-type plasminogen activator (PLAU), presenilin 1 (PSEN1), and CTSL that were upregulated in glioblastoma tissue compared to healthy brain tissue. The expression of specific elements of the IFN-γ pathway correlated with the expression of some of these proteases in glioblastoma samples. Moreover, IFN-γ affected the intracellular and extracellular levels of proteases (four were upregulated and six were downregulated) in glioblastoma-derived cells. Hence, IFN-γ signaling may play a role in glioblastoma by regulating the expression of some proteases. The CTSL protease was upregulated by IFN-γ and was associated with poor glioblastoma prognoses. Thus, we revealed a protease profile (ADAM9, CTSB, MMP7, CTSC, CTSL, MMP9, and PLAU) associated with glioblastoma progression and further demonstrated that CTSL is regulated by IFN-γ in glioblastoma cells. These results establish a link between IFN-γ signaling and protease regulation in glioblastoma.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"38-51"},"PeriodicalIF":1.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146061009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astilbin ameliorates propranolol-induced psoriasis-like lesions through restoring Th17/Treg immune homeostasis in lymph nodes.","authors":"Yayun Wu, Qi Xia, Dancai Fan, Ya Zhao, Lijuan Liu, Shigui Deng, Ruizhi Zhao","doi":"10.1684/ecn.2025.0505","DOIUrl":"https://doi.org/10.1684/ecn.2025.0505","url":null,"abstract":"<p><p>Psoriasis is a challenging immune-mediated dermatological disorder with an urgent need for effective clinical therapeutics, while astilbin has shown considerable efficacy in suppressing psoriasis progression, its underlying mechanisms are not fully clarified. This study aimed to systematically investigate the anti-psoriatic effects of astilbin and to elucidate its potential mechanisms of action. A psoriasis-like mouse model was established via cold water swimming, dietary restriction, and topical application of 5% propranolol emulsion, followed by daily treatment with low- (25.6 mg/kg), middle- (51.2 mg/kg), or high-dose (76.8 mg/kg) astilbin for 6 consecutive days, with evaluations including PASI scoring, histopathological examination, Baker scoring, inflammatory cytokine detection, and flow cytometric analysis of lymphocyte populations in lymph nodes and spleen. Middle and high doses of astilbin significantly reduced skin lesions and erythema, with PASI scores decreasing by 23.6%, and 44.9% respectively, Baker scores significantly reduced by 23.1% and 24.1% in the middle- and high-dose groups, and astilbin also significantly suppressed skin IL-17A, IL-6, and IFN-γ levels; moreover, middle and high doses substantially downregulated Th1, Th17, and Treg cell populations in lymph nodes and effectively restored Th17/Treg balance. Astilbin effectively ameliorates psoriatic skin lesions through immunomodulatory mechanisms involving the correction of lymph node Th17/Treg imbalance, highlighting its potential as a therapeutic agent for psoriasis.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 3","pages":"52-63"},"PeriodicalIF":1.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 IL-33 in immunotherapy for breast cancer: targets and signalling pathways.","authors":"Fu Zhang, Miao Lin, Yuancong Jiang, Fangjian Zhou","doi":"10.1684/ecn.2025.0500","DOIUrl":"https://doi.org/10.1684/ecn.2025.0500","url":null,"abstract":"<p><p>Interleukin-33 (IL-33), a key member of the IL-1 family, plays a significant role in inflammation and cancer. Its classic receptors, ST2 and IL-1 receptor accessory protein (IL-1RAcP), are predominantly expressed in immune cells such as T helper 2 (Th2) cells and mast cells. Recent studies have highlighted the involvement of IL-33 in breast cancer, demonstrating its ability to exert dual functional effects by modulating both innate and adaptive immune responses within the tumour microenvironment. However, the precise molecular mechanisms linking IL-33 to breast cancer pathogenesis and its potential as a target for molecularly targeted therapies remain incompletely understood. This review aims to provide a comprehensive summary of the current understanding of IL-33 in breast cancer immunotherapy.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 1","pages":"1-5"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"It’s in the blood: plasma as a source for biochemical identification and biological characterization of novel leukocyte chemoattractants.","authors":"Jo Van Damme, Stijn Van Damme, Sofie Struyf, Ghislain Opdenakker","doi":"10.1684/ecn.2025.0501","DOIUrl":"https://doi.org/10.1684/ecn.2025.0501","url":null,"abstract":"<p><p>Since their discovery, chemotactic cytokines or chemokines have been intensively studied for about half a century. Chemokines originate from tissue cells, leukocytes, blood platelets and plasma. Here, we review a number of seminal findings on plasma chemokines within an historical and international context. These aspects include how induction and purification protocols led to the discovery of a new family of mediators, named chemokines, on the basis of protein sequencing; how molecular cloning techniques facilitated discoveries of additional family members on the basis of conserved protein structures; how blood plasma and platelets were used as a source of inducible and constitutively expressed chemokines; how various forms of proteolytic reactions may convert precursor proteins into chemokines and either potentiate or inactivate their activity; how abundancy classes and synergism should be interpreted through critically considering plasma chemokine biology; and how other blood proteins, such as serum amyloid A, interact in functional terms with CXC and CC chemokines. The gradual dissection of all these elements not only reveals the complexity of chemokine actions, but also stimulates a more comprehensive interpretation of chemokine levels in plasma and serum, with future chemokinome analyses in mind.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"36 1","pages":"6-14"},"PeriodicalIF":2.2,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}