European cytokine network最新文献

{"title":"Toll-like receptor agonists, poly(I:C) and flagellin, lead to IL-36γ induction with divergent release kinetics and differentially alter autophagy in primary human keratinocytes","authors":"Christopher J Papayannakos,&nbsp;Daniel Zhu,&nbsp;Bongseok Jung,&nbsp;Ali A Rana,&nbsp;James A DeVoti,&nbsp;Allan L Abramson,&nbsp;Vincent R Bonagura,&nbsp;Bettie M Steinberg","doi":"10.1684/ecn.2022.0479","DOIUrl":"https://doi.org/10.1684/ecn.2022.0479","url":null,"abstract":"<p><p>IL-36γ, a pro-inflammatory member of the IL-1 cytokine superfamily, can be induced and secreted by normal human foreskin keratinocytes (HFKs) in response to pathogenic stimuli, however, the mechanisms underlying the secretion are unknown. In this study, we demonstrate that stimulation with the TLR3 agonist, poly (I:C), led to a delayed secretion of IL-36γ compared to stimulation with the TLR5 agonist, flagellin, despite equal levels of the cytokine (p = 0.006). IL-36γ was shown to be released from HFKs in its inactive, uncleaved form, based on western blotting. Moreover, recombinant IL-36γ in its activated, cleaved form induced endogenous IL-36γ 10-fold (p = 0.004) and CXCL8 five-fold (p = 0.003) over baseline levels compared to unactivated full-length recombinant IL-36γ. The ratio of LC3b-II/LC3b-I was significantly higher in poly(I:C)-treated cells compared to flagellin-treated and unstimulated controls without a change in SQSTM1/p62 after 24 hours of stimulation (p = 0.043). Under fluorescence microscopy, poly(I:C) led to a two-fold increase at eight hours and four-fold increase at 24 hours in accumulated autophagosomes post-stimulation (p = 0.032). In contrast, autophagosomes were unchanged relative to baseline in response to flagellin. Bafilomycin A1 treatment enhanced poly(I:C)-mediated IL-36γ secretion (p = 0.044) while rapamycin led to a noticeable, but non-significant, increase in flagellin-mediated IL-36γ secretion, indicating that interrupting autophagic flux can alter IL-3γ grelease from HFKs. Finally, we show that, compared to clinically normal laryngeal tissue, there were significantly higher levels of LC3b-II in HPV-infected respiratory papilloma tissue, indicating a higher number of autophagosomes; a signature of disrupted autophagic flux.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"33 2","pages":"43-53"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9117728","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":"Th1 cytokine endotype discriminates and predicts severe complications in COVID-19","authors":"Takehiro Hasegawa,&nbsp;Takashi Hato,&nbsp;Toshitsugu Okayama,&nbsp;Kazuho Ikeo,&nbsp;Yoshiaki Miyamoto,&nbsp;Niina Iwanaga,&nbsp;Kohjin Suzuki,&nbsp;Maho Yoshida,&nbsp;Kazuto Yamashita,&nbsp;Saya Yamashita,&nbsp;Eiya Tamada,&nbsp;Abdullah Khasawneh,&nbsp;Faith Jessica Paran,&nbsp;Rieko Oyama,&nbsp;Toshio Naito,&nbsp;Kenta Noda,&nbsp;Yoko Tabe","doi":"10.1684/ecn.2022.0477","DOIUrl":"https://doi.org/10.1684/ecn.2022.0477","url":null,"abstract":"<p><p>Treatment of severe and critical cases of coronavirus disease 2019 (COVID-19) is still a top priority in public health. Previously, we reported distinct Th1 cytokines related to the pathophysiology of severe COVID-19 condition. In the present study, we investigated the association of Th1 and Th2 cytokine/chemokine endotypes with cell-mediated immunity via multiplex immunophenotyping, single-cell RNA-Seq analysis of peripheral blood mononuclear cells, and analysis of the clinical features of COVID-19 patients. Based on serum cytokine and systemic inflammatory markers, COVID-19 cases were classified into four clusters of increasing (I-IV) severity. Two prominent clusters were of interest and could be used as prognostic reference for a targeted treatment of severe COVID-19 cases. Cluster III reflected severe/critical pathology and was characterized by decreased in CCL17 levels and increase in IL-6, C-reactive protein CXCL9, IL-18, and IL-10 levels. The second cluster (Cluster II) showed mild to moderate pathology and was characterized by predominated CXCL9 and IL-18 levels, levels of IL-6 and CRP were relatively low. Cluster II patients received anti-inflammatory treatment in early-stage, which may have led prevent disease prognosis which is accompanied to IL-6 and CRP induction. In Cluster III, a decrease in the proportion of effector T cells with signs of T cell exhaustion was observed. This study highlights the mechanisms of endotype clustering based on specific inflammatory markers in related the clinical outcome of COVID-19.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"33 2","pages":"25-36"},"PeriodicalIF":2.8,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9595088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9117725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of effective factors on IL-10 signaling in B cells in patients with selective IgA deficiency","authors":"Yasser Bagheri,&nbsp;Mohsen Saeidi,&nbsp;Reza Yazdani,&nbsp;Fateme Babaha,&nbsp;Reza Falak,&nbsp;Gholamreza Azizi,&nbsp;Marjan Taherian,&nbsp;Fereshteh Salami,&nbsp;Yaghoob Yazdani,&nbsp;Somayeh Sadani,&nbsp;Ali Hosseini,&nbsp;Morteza Motallebnezhad,&nbsp;Hassan Abolhassani,&nbsp;Mehdi Shekarabi,&nbsp;Asghar Aghamohammadi","doi":"10.1684/ecn.2021.0464","DOIUrl":"https://doi.org/10.1684/ecn.2021.0464","url":null,"abstract":"<p><strong>Background: </strong>Selective IgA deficiency is the most prevalent form of primary immunodeficiencies. The pathogenesis of the disease is still unknown. Several studies have suggested a defect in B cell responses to IL-10; however, the main reason for this defect has not been reported. Elucidating IL-10 signaling defects and their correlation with clinical manifestations could be helpful for better understanding and treatment of the disease.</p><p><strong>Methods: </strong>In this study, 15 SIgAD patients and 15 age- and sex-matched healthy controls were included. Surface expression of transforming growth factor β receptor II (TGF-β RII), IL-10R and IgA was assessed by flow cytometry in human purified B cells before and after stimulation by IL-10. Protein expression of STAT3, p-STAT3 and SOCS3 was measured by Western blotting analysis. TGF-β and IgA secretion was evaluated by ELISA. Finally, the measurement of B cell apoptosis was performed by flow cytometry.</p><p><strong>Results: </strong>The TGF-βRII expression level was decreased after stimulation with IL-10 in patients compared with controls. Notably, the TGF-β level were higher after stimulation with mCD40L and IL-10 in the control group as compared to stimulation with mCD40L alone. The IgA+ B cell percentage and IgA secretion levels were significantly increased in controls as compared with SIgAD patients. The relative concentration of the total STAT3 was decreased as compared with controls.</p><p><strong>Conclusion: </strong>The defect in IgA production in SIgAD patients could be due to inadequate B cell responses to IL-10 stimulation that probably originate from defective regulation of IL-10-mediated TGF-b ’symbol’ production TGF-β response by IL-10. Furthermore, it is suggested that the absence of STAT3 protein baseline expression could impair cytokine-mediated signaling such as thatinduced by IL-!0 and IL-21.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"33 1","pages":"1-12"},"PeriodicalIF":2.8,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40354499","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":"IL-27 attenuates airway inflammation and epithelial-mesenchymal transition in allergic asthmatic mice possibly via the RhoA/ROCK signalling pathway","authors":"Chuanjun Huang,&nbsp;Yan Sun,&nbsp;Na Liu,&nbsp;Ziping Zhang,&nbsp;Xiyan Wang,&nbsp;Degan Lu,&nbsp;Ling Zhou,&nbsp;Caiqing Zhang","doi":"10.1684/ecn.2021.0476","DOIUrl":"https://doi.org/10.1684/ecn.2021.0476","url":null,"abstract":"<p><strong>Background: </strong>Asthma is an airway disease characterized by airflow limitation and various additional clinical manifestations. Repeated inflammatory stimulation of the airways leads to epithelial-mesenchymal transition (EMT) which aggravates subepithelial fibrosis during the process of airway remodelling and enhances resistance to corticosteroids and bronchodilators in refractory asthma. There is growing evidence that IL-27 modulates airway remodelling, however, the molecular mechanisms involving IL-27 and EMT are poorly understood. The objective of this study was to investigate the effects of IL-27 on ovalbumin (OVA)-challenged asthmatic mice in vivo and TGF-β1-induced EMT in 16HBE cells in vitro.</p><p><strong>Methods: </strong>Airway inflammation, mucus secretion, and collagen deposition were analysed by conventional pathological techniques. The ratio of Th17 and Th9 cells in the spleen of mice was measured using flow cytometry, ELISA was performed for cytokine analysis to identify EMT-related molecules and signalling pathways, and other molecular and cellular techniques were used to explore the functional mechanism involving IL-27 and EMT.</p><p><strong>Results: </strong>Airway inflammation in asthmatic mice was significantly alleviated by IL-27, with downregulation of RhoA and ROCK, upregulation of E-cadherin, and a decrease of vimentin and α-SMA expression, compared to asthmatic mice. Moreover, the frequency of Th17 and Th9 cells in the spleen of asthmatic mice decreased following treatment with IL-27. In TGF-β1-induced 16HBE cells, the addition of IL-27 was shown to inhibit EMT, based on the expression of E-cadherin, vimentin, and α-SMA.</p><p><strong>Conclusion: </strong>Intranasal administration of IL-27 attenuates airway inflammation and EMT in a murine model of allergic asthma possibly by downregulating the RhoA/ROCK signalling pathway.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"33 1","pages":"13-24"},"PeriodicalIF":2.8,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40354500","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":"Metabolic link between obesity and autoimmune diseases.","authors":"Jacek Karczewski,&nbsp;Aleksandra Zielińska,&nbsp;Rafał Staszewski,&nbsp;Piotr Eder,&nbsp;Agnieszka Dobrowolska","doi":"10.1684/ecn.2021.0474","DOIUrl":"https://doi.org/10.1684/ecn.2021.0474","url":null,"abstract":"<p><p>The abnormal accumulation of visceral adipose tissue in obesity is associated with metabolic changes that include altered glucose tolerance, insulin resistance, hyperlipidemia, and metabolic syndrome. Obesity also coincides with increased incidence of autoimmune diseases. Accumulating evidence suggest that prolonged metabolic overload related to overnutrition, influenced by genetic and epigenetic factors, might affect immunologic self-tolerance through changes in the energy metabolism of immune cells, particularly regulatory T (Treg) cells. A strong activation of nutrient-energy signaling pathways blocks the induction of the transcription factor forkhead P3 (FOXP3), a master regulator of Treg cells, consequently inhibiting their generation and proliferation, thereby promoting proinflammatory response. Expanding our knowledge on the topic, particularly on metabolic T cell flexibility in vivo will provide new insights that can be used to develop therapeutic strategies for various inflammatory diseases, including obesity and autoimmune diseases. Targeting specific metabolic pathways is emerging as an important approach to control immune response and maintain immunological homeostasis.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 4","pages":"64-72"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39888557","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":"Post-COVID-19 arthritis: is it hyperinflammation or autoimmunity?","authors":"Sara Ibrahim Taha,&nbsp;Sara Farid Samaan,&nbsp;Rehab Ali Ibrahim,&nbsp;Eman Mousa El-Sehsah,&nbsp;Mariam Karam Youssef","doi":"10.1684/ecn.2021.0471","DOIUrl":"https://doi.org/10.1684/ecn.2021.0471","url":null,"abstract":"<p><strong>Background: </strong> Various musculoskeletal and autoimmune manifestations have been described in patients with coronavirus disease 2019 (COVID-19). Objectives: This study aims to investigate the prevalence and etiology of arthritis in post-COVID Egyptian patients. Methods: We included 100 post-COVID Egyptian patients who recovered 6 months ago and assessed several inflammatory and autoimmune markers. Results: The prevalence of post-COVID arthritis was 37%. Ankle, knee, and wrist were the most commonly affected joints. Old age (P = 0.010), smoking (P = 0.001), and arthralgia (P = 0.049) were all linked with post-COVID arthritis. Levels of pretreatment (baseline) interleukin (IL)-6 (46.41 ± 3.67 vs. 24.03 ± 2.46; P = 0.001), as well as 6-month post-COVID C-reactive protein (CRP; 98.49 ± 67.55 vs. 54.32 ± 65.73; P = 0.002), and erythrocyte sedimentation rate (ESR; 109.08 ± 174.91 vs. 58.35 ± 37.87; P = 0.029) were significantly higher in patients with arthritis compared to those without. On the other hand, complement C3 (P = 0.558) and C4 (P = 0.192), anti-nuclear antibodies (P = 0.709), and anti-cyclic citrullinated peptides (anti-CCP; P = 0.855) did not show significant differences. Only pretreatment IL-6 level was the significant single predictor of post-COVID arthritis with an odds ratio (95% confidence interval) of 3.988 (1.460-10.892) and a P-value of 0.007.</p><p><strong>Conclusion: </strong> The strong association observed with inflammatory markers (ESR and CRP) and the insignificant association with serologic markers of autoimmunity (ANA and anti-CCP) in our study support the notion that the underlying mechanism of post-COVID-19 arthritis is primarily due to the hyperinflammatory process associated with COVID-19 infection, and not the result of an autoimmune reaction. IL-6 levels before therapy can predict post-COVID arthritis allowing for early management.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 4","pages":"83-88"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8831681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39888558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-cytokine therapy and small molecule agents for the treatment of inflammatory bowel disease.","authors":"Yuancong Jiang,&nbsp;Deqiang Kong,&nbsp;Xiaolong Miao,&nbsp;Xing Yu,&nbsp;Zelai Wu,&nbsp;Han Liu,&nbsp;Weihua Gong","doi":"10.1684/ecn.2021.0472","DOIUrl":"https://doi.org/10.1684/ecn.2021.0472","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD), including Crohn disease and ulcerative colitis, with multifactorial etiologies has led to a global health-associated burden in many countries. Substantial efforts are devoted to understand the pathogenesis, behavioral and environmental triggers, which may be specifically valuable for the treatment of IBD. The specific pathogenesis underlying IBD is as yet incompletely understood. The use of anti-cytokine therapy and small molecule agents targeting the immune system is thought to restore the body's intestinal barrier function and relieve inflammation with manageable adverse effects. In this review, we report recent advances in anti-cytokine therapy and treatment with small molecule agents for the management of IBD.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 4","pages":"73-82"},"PeriodicalIF":2.8,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39888556","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":"Aberrant DNA methylation of the promoters of JAK2 and SOCS3 in juvenile systemic lupus erythematosus","authors":"Mahsa Keshavarz-Fathi, G. Sanati, M. Sadr, Bahareh Mohebbi, V. Ziaee, N. Rezaei","doi":"10.1684/ecn.2021.0469","DOIUrl":"https://doi.org/10.1684/ecn.2021.0469","url":null,"abstract":"Cytokine dysregulation is one of the important hallmarks of systemic lupus erythematosus (SLE) in both pediatric and adult patients. Owing to the substantial role of Janus kinase (JAK) and suppressor of cytokine signaling (SOCS) in cytokine signaling, we compared the methylation status of the promoter of JAK2 and SOCS3 between patients with JSLE and healthy controls. Peripheral blood samples were obtained from patients with JSLE and healthy controls. The promoter methylation was assessed by using the bisulfite conversion system and real-time quantitative multiplex methylation-specific PCR (QM-MSP). The methylation assessments were performed on the blood samples of 25 patients with JSLE and 24 healthy controls. The promoter of JAK2 was significantly hypomethylated in patients with JSLE compared to healthy controls. The median relative unmethylation of the promoter of JAK2 was higher in the JSLE group compared to the control group [0.44 (0.32,0.59) vs. 0.18 (0.12,0.86), respectively; P-value 0.026]. The promoter of SOCS3 was significantly hypermethylated in patients with JSLE compared to the controls. The median relative unmethylation of the promoter of SOCS3 was lower in the JSLE group compared to the control group [0.52 (0.10, 1.41) vs 1.18 (0.39, 2.19), respectively; P-value 0.032]. According to the results of our study, hypomethylation of the promoter of JAK2 and hypermethylation of the promoter of SOCS3 associate with JSLE. These alterations are possible mechanisms for activation of the JAK2 and suppression of the SOCS3 gene, respectively.","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 1","pages":"48 - 54"},"PeriodicalIF":2.8,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47428967","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":"Interleukin-17A serum levels in young patients with atopic dermatitis and food allergy","authors":"S. Baioumy, D. Sallam, S. Abdalgeleel, S. Fouad, Ahmed S. Khedr, Sara I. Taha","doi":"10.1684/ecn.2021.0470","DOIUrl":"https://doi.org/10.1684/ecn.2021.0470","url":null,"abstract":"Atopic dermatitis (AD) is a common skin disorder accompanied by skin barrier disruption. Patients with AD are commonly affected by food allergy. The present case-control study aimed to assess interleukin-17A (IL-17A) serum levels in children with AD and food allergies and to determine whether increased serum levels of this inflammatory cytokine correlate with disease severity. Healthy control subjects and patients were tested for food allergen reactivity by skin prick test and specific, as well as total, immunoglobulin E (IgE) analysis. IL-17A serum levels were measured by enzyme-linked immunosorbent assay technique. Patients with AD had significantly higher median (interquartile range) serum IL-17A (27 pg/mL [20–35] vs. 7 pg/mL [4.875–15.25]; P < 0.001) and total IgE levels (190 IU/mL [127–279] vs. 26.5 IU/mL [18.75–43.25]; P < 0.001) than controls and 44.6% (37/83) had a positive family history of allergy. Most patients with AD were reactive to two or three food allergens, with milk, eggs and nuts being the most common. No significant correlations were found between IL-17A levels and age and sex of patients, total IgE levels, the number and type of reactive food allergens and disease severity. In the receiver-operating characteristic analysis, the discriminating power of IL-17A and total IgE for AD severity was deficient when used alone but enhanced in combination. Serum IL-17A levels cannot be considered as a reliable AD severity measure and should be combined with other markers in a multimarker technique to enhance its predictive value.","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 1","pages":"55 - 63"},"PeriodicalIF":2.8,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47079045","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":"Upregulated Tie2 expression in plasma: a potential non-invasive biomarker for the diagnosis of breast cancer.","authors":"Qingzhu Song,&nbsp;Fenglan Zhang,&nbsp;Tian Yuan,&nbsp;Yulong Wei","doi":"10.1684/ecn.2021.0468","DOIUrl":"https://doi.org/10.1684/ecn.2021.0468","url":null,"abstract":"<p><p>Breast cancer is by far the most common malignancy found in women and causes a significant public health problem around the world. Early diagnosis of cancer plays an important role in successful treatment and survival of patients. This study aims to investigate the possibility of plasma Tie2 to be used as a biomarker for diagnosis of breast cancer. In total, 20 healthy volunteers and 33 breast cancer patients were considered for this study. The level of Tie2 in plasma was detected using the ELISA technique and immunohistochemistry was performed to measure the expression of Tie2 in normal and breast cancer tissues. Plasma concentrations of Tie2 were significantly higher among breast cancer patients compared to healthy subjects, and both mRNA and protein expression of Tie2 were higher in breast cancer tissue than in normal tissue. Plasma concentrations of Tie2 were positively correlated with the grade of breast cancer. Finally, in vitro knockdown of Tie2 expression in a breast adenocarcinoma cell line inhibited the proliferation of these cells. It is concluded from the results that Tie2 might be a useful plasma biomarker for the early detection of breast cancer and could be developed to be a target for novel drug discovery.</p>","PeriodicalId":11749,"journal":{"name":"European cytokine network","volume":"32 2","pages":"39-47"},"PeriodicalIF":2.8,"publicationDate":"2021-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39166839","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}