Journal of Interferon and Cytokine Research最新文献_第4页

Liquid-Liquid Phase Separation-Related STAT1 Modulating Ubiquitination Aggravates the Progression of Diabetic Nephropathy via Promoting Inflammatory Response. 液-液相分离相关STAT1调控泛素化通过促进炎症反应加重糖尿病肾病的进展

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-01-01 Epub Date: 2025-11-14 DOI: 10.1177/10799907251396047

Song Xue, Yingkui Si, Xue Han

{"title":"Liquid-Liquid Phase Separation-Related STAT1 Modulating Ubiquitination Aggravates the Progression of Diabetic Nephropathy via Promoting Inflammatory Response.","authors":"Song Xue, Yingkui Si, Xue Han","doi":"10.1177/10799907251396047","DOIUrl":"10.1177/10799907251396047","url":null,"abstract":"This study aims to screen liquid-liquid phase separation (LLPS)-related genes modulating ubiquitination for diagnosing patients with diabetic nephropathy (DN). After performing differential gene expression analysis, ssGSEA, and immune infiltration analysis, LLPS-related genes modulating ubiquitination, key immune cells, and immune-related pathways were acquired. The correlations between LLPS-related genes and ubiquitination, key immune-related pathways were explored, respectively. The diagnostic genes were identified by four machine learning algorithms, followed by evaluation to predict the performance of the machine learning models on ubiquitination using receiver operating characteristic curves and a confusion matrix. In vitro experiments were applied to explore the function of signal transducer and activator of transcription 1 (STAT1) in DN. Totally, 513 differentially expressed genes were screened between the DN and control groups. The activity of the ubiquitin-mediated proteolysis pathway exhibited a significant difference between the DN and control samples. The fraction of a total of 10 immune cells exhibited a significant difference between the lower and higher ubiquitination groups. Totally, nine LLPS-related genes modulating ubiquitination were acquired, and these genes modulating ubiquitination were enriched in ubiquitin pathways and significantly positively correlated with the complement, IFN-α, and IFN-γ pathways. Two diagnostic genes were obtained, namely dual specificity tyrosine phosphorylation regulated kinase 2 (DYRK2) and STAT1. Notably, downregulation of STAT1 effectively alleviated IFN-γ, IFN-α, IL-1β, and TNF-α levels in D-glucose-treated HK-2 cells, as well as the protein level of FK2. LLPS-related STAT1 modulating ubiquitination accelerates the inflammatory response in DN.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"1-10"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145564193","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}

引用次数: 0

Bushen Huoxue Acupuncture Suppresses the Release of Inflammation Cytokines in a Mouse Model of Neurodegenerative Disease by Modulating the SIRT2/RTN4B/BACE1 Pathway. 补肾活血针通过调节SIRT2/RTN4B/BACE1通路抑制神经退行性疾病小鼠模型中炎症细胞因子的释放

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-01-01 Epub Date: 2025-11-13 DOI: 10.1177/10799907251391519

Hongqin Li, Rong Xu, Liquan Xie, Weiguang Li, Xing Lin, Pin Yang

{"title":"Bushen Huoxue Acupuncture Suppresses the Release of Inflammation Cytokines in a Mouse Model of Neurodegenerative Disease by Modulating the SIRT2/RTN4B/BACE1 Pathway.","authors":"Hongqin Li, Rong Xu, Liquan Xie, Weiguang Li, Xing Lin, Pin Yang","doi":"10.1177/10799907251391519","DOIUrl":"10.1177/10799907251391519","url":null,"abstract":"Bushen Huoxue Acupuncture shows potential in treating neurodegenerative diseases, but its mechanisms remain incompletely understood. Using the senescence-accelerated mouse-prone 8 (SAMP8) mouse model, we assessed cognitive function via the Morris water maze test, hippocampal neuronal apoptosis with terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and microglial activation through immunohistochemistry. Serum levels of inflammatory cytokines [tumor necrosis factor-alpha, interleukin (IL)-1β, and IL-6] were quantified by enzyme-linked immunosorbent assay. The expression of SIRT2 pathway-related proteins, along with Aβ deposition, was analyzed using Western blotting, immunohistochemistry, and immunofluorescence. The results demonstrated that Bushen Huoxue Acupuncture improved cognitive function in SAMP8 mice, reducing hippocampal neuronal apoptosis and decreasing serum levels of pro-inflammatory cytokines. Additionally, it reduced the levels of Aβ42, a more aggregation-prone and toxic Aβ subtype, in both hippocampal tissues and serum, as well as the number of CD68-positive cells in hippocampal tissues, suggesting the inhibition of amyloid pathology and neuroinflammatory. The treatment also downregulated SIRT2, BACE1, and APP-CTF while increasing RTN4B expression. Notably, Bushen Huoxue Acupuncture outperformed non-acupoint acupuncture in enhancing cognitive function and reducing inflammation. Our findings indicate that Bushen Huoxue Acupuncture alleviates cognitive deficits and neuroinflammation by suppressing the SIRT2-mediated RTN4B/BACE1 pathway, highlighting acupuncture as a promising therapy for neurodegenerative diseases.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"22-31"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145541072","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}

引用次数: 0

Exosomes Derived from Platelet-Rich Plasma Facilitates Macrophage Mitophagy in Diabetic Wound Healing by Targeting KNG1 via PI3K-AKT Pathway. 富血小板血浆外泌体通过PI3K-AKT通路靶向KNG1促进糖尿病伤口愈合中的巨噬细胞自噬

IF 1.9 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2026-01-01 Epub Date: 2025-11-17 DOI: 10.1177/10799907251391527

Cao Han, Tao Zhong, Zhengnan Zhao, Yongxu Zhang, Haoran Cheng, Zhigang Sui, Haidong Liang, Zhuo Zhao

{"title":"Exosomes Derived from Platelet-Rich Plasma Facilitates Macrophage Mitophagy in Diabetic Wound Healing by Targeting KNG1 via PI3K-AKT Pathway.","authors":"Cao Han, Tao Zhong, Zhengnan Zhao, Yongxu Zhang, Haoran Cheng, Zhigang Sui, Haidong Liang, Zhuo Zhao","doi":"10.1177/10799907251391527","DOIUrl":"10.1177/10799907251391527","url":null,"abstract":"This study was conducted to investigate the protective effect of platelet-rich plasma-derived exosomes (PRP-Exos) in diabetic wound healing, as well as the involved molecular mechanism. Exosomes collected from PRP were extracted and identified, then the promoting effect on diabetic wound healing was tested in high glucose and lipopolysaccharide (HL)-induced RAW264.7 cells and excisional wound models constructed in streptozotocin-induced diabetic SD rats. PRP-Exos showed the best capacity for accelerating wound healing in the diabetic rat model. Cell proliferation of RAW264.7 cells was effectively facilitated after HL treatment, while PRP-Exos implemented could obviously eliminate the HL effect on RAW264.7 cells. The protein expression levels of PINK1, parkin, and LC3I/LC3II were both obviously diminished, and the expression of kininogen-1 (KNG1) was obviously increased in HL-induced RAW264.7 cells, while the opposite results were observed after PRP-Exos treatment. HL treatment could remarkably suppress the protein expression levels of p-PI3K/PI3K and p-AKT/AKT in RAW264.7 cells, while PRP-Exos administration could reverse this trend. Interestingly, KNG1 upregulation could effectively reverse the effect of PRP-Exos on the tumor necrosis factor-alpha and high mobility histone 1 levels, protein expression of p-PI3K/PI3K and p-AKT/AKT, and mitophagy-related markers in HL-induced RAW264.7 cells. In conclusion, PRP-Exos facilitated macrophage mitophagy in diabetic wound healing by targeting KNG1 via PI3K-AKT pathway.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"11-21"},"PeriodicalIF":1.9,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145564240","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}

引用次数: 0

Severe Impairment of IFN-α and IFN-γ Responses in Cells of a Patient with a Rare STAT1 Tail Segment Domain Mutation. 罕见的STAT1尾段结构域突变患者细胞中IFN-α和IFN-γ反应严重受损

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-12-01 Epub Date: 2025-10-20 DOI: 10.1177/10799907251389756

Jing Xiao, Jiapeng Qiu

{"title":"Severe Impairment of IFN-α and IFN-γ Responses in Cells of a Patient with a Rare STAT1 Tail Segment Domain Mutation.","authors":"Jing Xiao, Jiapeng Qiu","doi":"10.1177/10799907251389756","DOIUrl":"10.1177/10799907251389756","url":null,"abstract":"Signal transducer and activator of transcription 1 (STAT1) mutations are associated with diverse pathologies. Loss-of-function (LOF) heterozygous mutations impair interferon (IFN) signaling, predisposing to Mendelian susceptibility to mycobacterial diseases (MSMDs). This study characterizes a novel STAT1 LOF mutation in a patient with multisystem manifestations. A patient presenting with mycobacterial infection, skeletal abnormalities, and systemic inflammation underwent whole-exome sequencing. The identified STAT1 variant was analyzed via computational tools (PolyPhen-2/SIFT). Molecular biological validation included IFN-α/γ-induced STAT1 phosphorylation assays and fluorescence microscopy for subcellular localization. Clinical features included mycobacterial osteomyelitis, severe rash, dwarfism, hepatosplenomegaly, and elevated inflammatory markers (C-reactive protein/erythrocyte sedimentation rate). A heterozygous STAT1 mutation (NM_007315.4:c.2120T>C; p.Ile707Thr) was identified and predicted as pathogenic. Mutant cells showed reduced STAT1 phosphorylation (64% versus wild-type, P < 0.05) and impaired nuclear translocation post-IFN-α/γ stimulation. Antibiotic therapy achieved clinical resolution without complications. These findings indicated that the STAT1 I707T mutation disrupts IFN-α/γ immunity, expanding the MSMD genotypic spectrum. Genetic screening for STAT1 defects is critical in patients with mycobacterial infections involving skin. Molecular biological studies corroborate mutation pathogenicity, guiding therapeutic decisions.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"385-393"},"PeriodicalIF":1.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145337171","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}

引用次数: 0

Lnc-HSFY2-10:1 Contributes to Keratinocyte Proliferation and Psoriatic Inflammation Through miR-145-5p/FN1 Axis. Lnc-HSFY2-10:1通过miR-145-5p/FN1轴参与角质细胞增殖和银屑病炎症

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-12-01 Epub Date: 2025-09-15 DOI: 10.1177/10799907251376857

Luan Yang, Ruijie Wang, Yingying Sun, Zhenqiang Ruan, Haiyan Jia, Jianjun Yan

{"title":"Lnc-HSFY2-10:1 Contributes to Keratinocyte Proliferation and Psoriatic Inflammation Through miR-145-5p/FN1 Axis.","authors":"Luan Yang, Ruijie Wang, Yingying Sun, Zhenqiang Ruan, Haiyan Jia, Jianjun Yan","doi":"10.1177/10799907251376857","DOIUrl":"10.1177/10799907251376857","url":null,"abstract":"Psoriasis is an immune-mediated chronic inflammatory disease characterized by keratinocyte hyperproliferation and inflammatory cell infiltration. While noncoding RNAs are implicated in its progression, research remains limited. Integrating lncRNA microarray data with LncRNASNP2-based predictions identified the long noncoding RNA (lncRNA) HSFY2-10:1 as a potential functional lncRNA contributing to psoriasis pathogenesis. This study aimed to investigate the role of lnc-HSFY2-10:1/miR-145-5p/fibronectin (FN1) axis in psoriasis. We found that HSFY2-10:1 was significantly upregulated in psoriatic tissues. In a psoriasis cell model established by stimulating NHEKs and HaCaT cells with the M5 cytokine cocktail (IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α), lnc-HSFY2-10:1 promoted keratinocyte hyperproliferation and CCL20 secretion. Mechanistically, HSFY2-10:1 functioned as a competitive endogenous RNA for miR-145-5p, thereby regulating FN1 expression. Overexpression of miR-145-5p markedly reversed the HSFY2-10:1-induced upregulation of FN1, keratinocyte proliferation, and CCL20 secretion. These findings indicate that the lnc-HSFY2-10:1/miR-145-5p/FN1 axis plays a crucial role in psoriasis pathogenesis and serves as a potential therapeutic target. [Figure: see text].","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"375-384"},"PeriodicalIF":1.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145064825","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}

引用次数: 0

A Conversation with Alex Lercher. 与Alex Lercher的对话。

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-11-01 Epub Date: 2025-10-17 DOI: 10.1177/10799907251390651

Alexander Lercher

引用次数: 0

Immunomodulatory Effects of Ticagrelor in Myocardial Infarction: Shifting the Cytokine Balance Toward an Anti-Inflammatory Profile. 替格瑞洛在心肌梗死中的免疫调节作用：将细胞因子平衡向抗炎方向转移。

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-11-01 Epub Date: 2025-11-05 DOI: 10.1177/10799907251394220

Delan Yaseen Sulaiman, Talar Ahmad Merza Mohammad

{"title":"Immunomodulatory Effects of Ticagrelor in Myocardial Infarction: Shifting the Cytokine Balance Toward an Anti-Inflammatory Profile.","authors":"Delan Yaseen Sulaiman, Talar Ahmad Merza Mohammad","doi":"10.1177/10799907251394220","DOIUrl":"10.1177/10799907251394220","url":null,"abstract":"Myocardial infarction (MI) triggers a systemic inflammatory response that influences cardiac recovery. Pharmacological therapies, including aspirin, β-blockers, Angiotensin-Converting Enzyme (ACE) inhibitors, statins, and P2Y12 inhibitors such as Ticagrelor, may have additional immunomodulatory effects beyond their primary cardiovascular benefits. This study evaluates the impact of different treatment regimens on inflammatory markers, immune cell phenotyping, and cardiac biomarkers in MI patients. A total of 78 MI patients were divided into three treatment groups: standard therapy (aspirin + β-blockers), enhanced therapy (aspirin, β-blockers, ACE inhibitors, and statins), and experimental therapy (Ticagrelor + standard therapy). Inflammatory cytokines (Interleukin (IL)-4, IL-6, IL-10, IL-17, Interferon (IFN)-γ, Tumor Necrosis Factor (TNF)-α, Transforming Growth Factor (TGF)-β), cardiac biomarkers [Troponin, B-type natriuretic peptide (BNP)], and immune cell profiles (Th1/Th2 balance) were assessed using Enzyme-Linked Immunosorbent Assay (ELISA), qPCR (Polymerase Chain Reaction), and flow cytometry before and after treatment. Pro-inflammatory markers (IL-6, TNF-α, IFN-γ, IL-17) significantly decreased, while anti-inflammatory cytokines (IL-4, IL-10, TGF-β) increased post-treatment (P < 0.0001). Th1 cell proportions declined, with a concurrent rise in Th2 cells, particularly in enhanced and experimental therapy groups. Troponin and BNP levels decreased, indicating reduced myocardial stress. Pharmacological therapies effectively modulate immune responses, suppress inflammation, and promote myocardial recovery. Ticagrelor demonstrated additional anti-inflammatory benefits, suggesting potential for improved post-MI outcomes. Future studies should explore long-term clinical implications of immune-targeted cardiovascular therapy.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"365-374"},"PeriodicalIF":1.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145451527","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}

引用次数: 0

A Conversation with Autumn York. 对谈秋·约克。

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-11-01 Epub Date: 2025-11-06 DOI: 10.1177/10799907251395956

Autumn York

引用次数: 0

Hirudin Inhibits Pyroptosis to Alleviate Renal Fibrosis via the mTOR/HIF-1α Pathway. 水蛭素通过mTOR/HIF-1α途径抑制焦亡减轻肾纤维化。

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-10-01 Epub Date: 2025-09-08 DOI: 10.1177/10799907251374414

Chunli Long, Jiefang Chen, Yongxiang Xie

{"title":"Hirudin Inhibits Pyroptosis to Alleviate Renal Fibrosis via the mTOR/HIF-1α Pathway.","authors":"Chunli Long, Jiefang Chen, Yongxiang Xie","doi":"10.1177/10799907251374414","DOIUrl":"10.1177/10799907251374414","url":null,"abstract":"Hirudin, a polypeptide extracted from medicinal leeches, has demonstrated potential in treating renal fibrosis. This study aimed to explore the underlying mechanisms by which Hirudin alleviates renal fibrosis. Renal fibrosis models were established using unilateral ureteral obstruction (UUO) surgery in rats and transforming growth factor-β (TGF-β)-induced HK-2 cells, followed by treatment with different concentrations of Hirudin. Renal function indicators were detected using an automatic analyzer. Renal pathology was observed using hematoxylin-eosin and Masson staining, and α-smooth muscle actin (α-SMA) (a fibrosis marker) expression was detected by immunohistochemistry. Cell viability was tested using cell counting kit-8 assay. Western blot was utilized to detect α-SMA, NOD-like receptor thermal protein domain associated protein 3 (NLRP3), Gasdermin D (GSDMD), cleaved caspase-1, phosphorylated mammalian target of rapamycin (p-mTOR), mammalian target of rapamycin (mTOR), and hypoxia-inducible factor-1α (HIF-1α) levels. Interleukin (IL)-1β and IL-18 levels were measured using enzyme-linked immunosorbent assay (ELISA). UUO rats exhibited impaired renal function and severe renal fibrosis, accompanied by increased NLRP3, GSDMD, cleaved caspase-1, IL-1β, IL-18, p-mTOR/mTOR, and HIF-1α levels. Hirudin alleviated renal fibrosis, reduced pyroptosis, and inhibited mTOR/HIF-1α pathway in UUO rats. TGF-β stimulation decreased cell viability, increased α-SMA expression and pyroptosis, and activated mTOR/HIF-1α pathway in HK-2 cells. These changes were reversed by Hirudin. However, the mTOR agonist MHY1485 altered the effects of Hirudin. In conclusion, Hirudin reduces pyroptosis to alleviate renal fibrosis, potentially by suppressing mTOR/HIF-1α pathway.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"335-343"},"PeriodicalIF":1.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015561","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}

引用次数: 0

CXCR 4, PAX5, and OCT2 Immunohistochemical Expressions in Diffuse Large B-Cell Lymphoma and Their Relationship with XIST/miR-34/PAX5 Axis. 弥漫性大b细胞淋巴瘤中cxcr4、PAX5和OCT2免疫组织化学表达及其与XIST/miR-34/PAX5轴的关系

IF 1.8 4区医学

Journal of Interferon and Cytokine Research Pub Date : 2025-10-01 Epub Date: 2025-09-26 DOI: 10.1177/10799907251379845

Noha F Elaidy, Samia Hussein, Hoda F Ebian, Maha Mahmoud Hamed Sakr, Ahmad Barakat Waley, Doaa M Hendawy, Heba Mahmoud Abdelgeleel, Reham Sameh

{"title":"CXCR 4, PAX5, and OCT2 Immunohistochemical Expressions in Diffuse Large B-Cell Lymphoma and Their Relationship with XIST/miR-34/PAX5 Axis.","authors":"Noha F Elaidy, Samia Hussein, Hoda F Ebian, Maha Mahmoud Hamed Sakr, Ahmad Barakat Waley, Doaa M Hendawy, Heba Mahmoud Abdelgeleel, Reham Sameh","doi":"10.1177/10799907251379845","DOIUrl":"10.1177/10799907251379845","url":null,"abstract":"C-X-C chemokine receptor 4 (CXCR4) is a chemokine receptor. Paired box protein 5 (PAX5) is a nuclear transcription factor. Octamer-binding protein 2 (OCT2) is a B-cell-restricted transcription factor. This study aimed to evaluate the protein expression of CXCR4, PAX5, and OCT2, as well as the gene expression of long noncoding RNA (lncRNA) X-inactive specific transcript (XIST)/miR-34/PAX5, in diffuse large B-cell lymphoma (DLBCL). The study included 67 patients with DLBCL and 15 lymphoid tissue samples from reactive lymph nodes. Immunohistochemical (IHC) methods were used to evaluate protein expression. Gene expression was measured by real-time polymerase chain reaction. Correlation analysis showed significant negative correlations between miR-34 expression and each of the XIST expression (r = -0.41, P < 0.001) and PAX5 expression (r = -0.43, P < 0.001). At the same time, there was a strong positive correlation between XIST expression and PAX5 expression (r = 0.92, P < 0.001). In conclusion, our findings indicate that CXCR4, OCT2, and PAX5 IHC expressions can be considered diagnostic markers in DLBCL. In addition, the XIST/miR-34/PAX5 axis may serve as a potential diagnostic marker in DLBCL. Moreover, CXCR4 and XIST/miR-34/PAX5 expressions may be potential prognostic markers in DLBCL.","PeriodicalId":16261,"journal":{"name":"Journal of Interferon and Cytokine Research","volume":" ","pages":"344-359"},"PeriodicalIF":1.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145176068","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}

引用次数: 0