BMC Immunology最新文献

{"title":"Elevated CDYL expression in the peripheral blood of patients with rheumatoid arthritis.","authors":"Mengxue Xu, Xueli Xia, Jun Yang, Lin Zhao, Juan Xu, Shengjun Wang, Dawei Cui, Huiyong Peng","doi":"10.1186/s12865-026-00847-3","DOIUrl":"10.1186/s12865-026-00847-3","url":null,"abstract":"<p><strong>Background: </strong>Chromodomain Y-like protein (CDYL), a member of the CDY-related gene family, plays a pivotal role in nervous diseases, reproductive systems and tumors by chromatin remodeling and disrupting normal transcriptional regulation. However, the expression and biological functions of CDYL in rheumatoid arthritis (RA) remain unclear. This study aims to investigated the role of CDYL in the pathogenesis of RA.</p><p><strong>Methods: </strong>A cohort of 43 RA patients and 36 healthy subjects were included in the study. The transcript levels of CDYL, interleukin-17 A (IL-17 A) and IL-22 were detected by quantitative real-time PCR. Flow cytometry and Western blot were used to analyze the relationship between CDYL and Th17 cells. The GSE100191 dataset from the GEO database was downloaded to conduct a comprehensive bioinformatics analysis of the potential functions of CDYL. The interaction of CDYL and EZH2 and the effects of the EZH2 antagonist on Th17 cells were measured by Western blot.</p><p><strong>Results: </strong>The CDYL was highly expressed in the PBMCs derived from RA patients, exhibiting positive correlations with DAS28 score (r = 0.36, p < 0.0177) and serum anti-cyclic citrullinated peptide antibody titers (r = 0.4255, p = 0.004). Moreover, the transcript levels of CDYL were positively correlated with elevated IL-17 A levels (r = 0.5140, p < 0.001) and IL-22 (r = 0.4540, p = 0.002) levels in RA patients and the RA dataset. CDYL expression is markedly upregulated in Th17 cells, while the proportion of Th17 cells is increased in RA patients. Mechanistically, CDYL knockdown significantly inhibited Th17 differentiation in vitro, which suggests that CDYL is associated with and functionally contributes to the differentiation of Th17 cells.</p><p><strong>Conclusions: </strong>Our findings indicate that CDYL expression is associated with and promotes the differentiation of Th17 cells in RA patients and may be involved in the process of RA.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13383126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004499","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":"Genetic susceptibility and HLA association in autoimmune hepatitis among Yemeni patients.","authors":"Waleed Qassem Farie, Saleh Salem Bahaj, Anwar Kassem Al-Madhagi, Sarosh Sher Ali, Aref Noman, Waleed Yahya Alkassar","doi":"10.1186/s12865-026-00838-4","DOIUrl":"10.1186/s12865-026-00838-4","url":null,"abstract":"<p><strong>Background: </strong>Autoimmune hepatitis (AIH) is a chronic, immune-mediated liver disease characterized by the progressive destruction of hepatocytes, often leading to cirrhosis and liver failure. Genetic predisposition, particularly the involvement of human leukocyte antigen (HLA) alleles, is well-documented in the pathogenesis of AIH. However, the specific HLA associations in the Yemeni population remain unexplored, despite increasing clinical evidence of AIH in this region.</p><p><strong>Objective: </strong>This study aims to elucidate the distribution of HLA class alleles in Yemeni patients (aged ≥ 18 years) with AIH and assess their association with disease susceptibility, contributing to the growing body of immunogenetic research in Middle Eastern populations.</p><p><strong>Methods: </strong>This case-control study included 93 AIH patients and 280 healthy controls (total N = 373), all of Yemeni origin. We conducted high-resolution HLA typing and compared the frequencies of HLA alleles with global data. Allelic distributions were analyzed for associations with AIH susceptibility, and findings were interpreted in the context of previously identified genetic markers of autoimmune liver disease.</p><p><strong>Results: </strong>The most frequent allele in Yemeni AIH patients was HLA-DRB1*03:01 (42.5% vs. 15.5% in controls, OR = 4.0, 95% CI = 2.8-5.8, p = 0.01), followed by HLA-DRB1*04:01 (21.5% vs. 16.9%, OR = 1.3, 95% CI = 1.1-2.0, p = 0.04) and HLA-A*02 (31.7% vs. 27.9%, OR = 1.2, 95% CI = 1.1-1.3, p = 0.001). Protective alleles such as HLA-DRB1*13:01 were significantly more frequent in controls (13.2% vs. 3.8%, OR = 0.3, 95% CI = 0.1-0.6, p = 0.001). Our results demonstrate a genetic predisposition to AIH in Yemen, primarily associated with the HLA-DRB1*03:01 and HLA-DRB1*04:01 alleles. The observed distribution aligns with international trends but also reveals distinct ethnic-specific patterns that warrant further investigation.</p><p><strong>Conclusion: </strong>This study highlights the critical role of HLA-DRB1* alleles, particularly DRB1*03:01 and DRB1*04:01, in the genetic susceptibility to AIH in the Yemeni population. These findings not only enhance the understanding of genetic factors in AIH but also establish a foundation for future immunogenetic research in the Middle East. The identification of region-specific HLA associations could inform both diagnostic and therapeutic strategies for AIH in Yemen and similar populations. This study was restricted to adults (≥ 18 years); therefore, findings may not apply to pediatric AIH.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980384","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":"IL-21 rs2055979 and serum IL-21 levels are associated with both non-segmental and segmental vitiligo in an Iranian cohort.","authors":"Nasser Gholijani, Zeinab Dehghan, Samira Sadat Abolmaali, Atefe Ghamar Talepoor, Mohammadreza Yazdani, Gholamreza Daryabor","doi":"10.1186/s12865-026-00846-4","DOIUrl":"10.1186/s12865-026-00846-4","url":null,"abstract":"<p><strong>Background: </strong>Vitiligo is an autoimmune disorder primarily categorized into non-segmental (NSV) and segmental (SV) subtypes. Interleukin-21 (IL-21) is a pleiotropic cytokine implicated in immune dysregulation.</p><p><strong>Objective: </strong>To investigate the association of serum IL-21 levels and two genetic variants (rs2055979 and rs4833837) with susceptibility to NSV and SV in an Iranian cohort.</p><p><strong>Methods: </strong>The study included 264 vitiligo patients (225 NSV, 39 SV) and up to 390 healthy controls. Serum IL-21 was measured by ELISA. Genotyping for rs2055979 was performed by RFLP-PCR, and for rs4833837 by ASO-PCR.</p><p><strong>Results: </strong>Serum IL-21 levels were significantly elevated in both NSV (median 71.50 pg/mL) and SV (median 65.35 pg/mL) patients compared to controls (median 18.70 pg/mL; p < 0.0001). For rs2055979, the GT genotype was associated with increased risk of NSV (unadjusted OR = 2.99, 95% CI = 1.86-4.80, p < 0.0001; age- and sex-adjusted OR = 1.809, 95% CI = 1.061-3.085, p = 0.029) and SV (unadjusted OR = 4.29, 95% CI = 1.45-12.7, p = 0.005; adjusted OR = 3.486, 95% CI = 1.006-12.077, p = 0.049). The unadjusted G allele was a risk factor for NSV (OR = 1.52, 95% CI = 1.19-1.94, p = 0.0009) but not for SV (p = 0.09). The GG genotype also conferred elevated unadjusted risk for NSV (OR = 2.51, 95% CI = 1.44-4.37, p = 0.0009). In contrast, rs4833837 showed no significant association with either vitiligo subtype.</p><p><strong>Conclusion: </strong>The IL-21 rs2055979 polymorphism is associated with vitiligo susceptibility, with the GT genotype representing a risk factor for both NSV and SV after adjustment for age and sex. The marked elevation of serum IL-21 in both NSV and SV further supports a pathogenic role for IL-21, suggesting the IL-21/IL-21R axis as a potential therapeutic target.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13374329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147962225","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":"Clinical applications and methodology updates in HLA typing.","authors":"Kaihao Feng, Le Chang, Ying Yan, Huizhen Sun, Yi Liu, Shi Song, Abudulimutailipu Nuermaimaiti, Shana Halemubieke, Ling Mei, Qian Su, Xinru Liu, Zhuoqun Lu, Huimin Ji, Lunan Wang","doi":"10.1186/s12865-026-00845-5","DOIUrl":"10.1186/s12865-026-00845-5","url":null,"abstract":"<p><p>The Human Leukocyte Antigen (HLA) system is a key component of the immune system, involving aspects such as autoimmune reactions, transplant rejection reactions, and related diseases. HLA typing technology enables precise decision-making in clinical tissue matching, disease susceptibility assessment, and drug response prediction. Therefore, this article summarizes the genetic characteristics of HLA, several commonly used methods for typing, including serological methods and molecular biology methods. It also explores the clinical applications of HLA typing, such as in organ and stem cell transplantation, blood transfusion, and disease association studies. In addition, in recent years, the combination of Single Nucleotide Polymorphism (SNP) and PCR technology has shown its potential application in various gene typing. In particular, the application of SNP-PCR method in HLA typing provides new possibilities for improving typing accuracy, reducing costs, and shortening detection time. Therefore, we summarize the existing HLA typing technologies and prospects for the future development of SNP-PCR method in HLA typing. With the continuous progress of bioinformatics and high-throughput sequencing technology, SNP-PCR is expected to become an efficient, economical, and widely used method for HLA typing, providing strong support for precision medicine. In addition, combined with big data analysis, SNP-PCR is expected to further reveal the complex associations between HLA and various diseases, thereby promoting in-depth research and development in immunology, genetics, and clinical medicine.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13374135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940031","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":"Treponema pallidum induces pathological injury of the rabbit testis and sperm through NLRP3 inflammasome activation-mediated pyroptosis.","authors":"Tong Zheng, Meiping Ye, Yilan Yang, Linxin Yao, Danyang Zou, Chunjie Liao, Xin Feng, Tingli Tian, Zhuojun Tang, Pingyu Zhou","doi":"10.1186/s12865-026-00835-7","DOIUrl":"10.1186/s12865-026-00835-7","url":null,"abstract":"<p><strong>Background: </strong>Treponema pallidum (T. pallidum) can invade various organs and tissues. However, there have been few studies on the pathological injury of T. pallidum to the testis and sperm. The NOD-like receptor protein 3 (NLRP3) inflammasome, upon activation, leads to pyroptosis-a programmed, pro-inflammatory cell death process, and promotes inflammatory responses. Previous investigations have found that the NLRP3 inflammasome is elevated in the testis tissues of rabbits infected with T. pallidum. This study aimed to investigate whether T. pallidum induced pathological injury of the rabbit testis and sperm through NLRP3 inflammasome-mediated pyroptosis.</p><p><strong>Methods: </strong>While rabbits in the T. pallidum group received an intratesticular injection of 1 mL of a bacterial suspension containing 10⁷/mL treponemes, those in the sham group were administered an equal volume of normal saline to serve as the injection procedure control. 14 days later, testis tissues were harvested for IHC and H&E staining, and analysis of qPCR. In vitro, GC-2spd cells were stimulated by T. pallidum (MOI = 20). After administering MCC950, the expression levels of the inflammasome NLRP3 and downstream pyroptosis-related molecules were subsequently detected.</p><p><strong>Results: </strong>T. pallidum caused obvious pathological damage to the rabbit testis and sperm reduction. Meanwhile, the gene expression levels of NLRP3, ASC, GSDMD, Caspase-1, IL-Iβ, and IL-18 in the T. pallidum group were higher than those of the sham group. Additionally, T. pallidum induced cell injury and pyroptosis in GC-2spd cells, which was improved by the NLRP3 inflammasome inhibitor MCC950.</p><p><strong>Conclusions: </strong>Our findings validated that T. pallidum induced pathological damage to the testis and sperm reduction via NLRP3 inflammasome activation and pyroptosis. By specifically inhibiting the NLRP3 inflammasome, MCC950 has the potential to ameliorate sperm cell damage under in vitro conditions via the blockade of pyroptotic cell death.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855861","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":"Extracellular vesicles from miR-146a-overexpressing mesenchymal stem cells reduce ligature-induced periodontitis by modulating inflammatory cytokines.","authors":"Wen Chu, Yinuo Zhang, Shiying Shen, Zhilu Wang, Yanxu Guo, Yanfang Yu, Dahai Huang, Nara Davtyan","doi":"10.1186/s12865-026-00839-3","DOIUrl":"10.1186/s12865-026-00839-3","url":null,"abstract":"<p><strong>Background: </strong>Periodontitis is a long-lasting inflammatory disorder of structures attached, which is significantly influenced by insufficient or dysregulated immune responses. Mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) are a promising therapeutic modality. This study explores the therapeutic efficacy of EVs derived from miR-146a-overexpressing bone marrow-derived mesenchymal stem cells (BMSCs) in a ligature-induced periodontitis model.</p><p><strong>Results: </strong>BMSCs were transfected to overexpress miR-146a, and their EVs were isolated. Periodontitis was induced in 30 female C57Bl/6 mice and divided into three groups: a control group receiving PBS, a miR-control EV-treated group, and a miR-146a-EV-treated group. EVs were administered subgingivally, and clinical parameters were evaluated. Levels of proinflammatory cytokines interleukin (IL)-1β, IL-8, tumor necrosis factor (TNF)-α, and IL-6, as well as anti-inflammatory cytokines IL-10, IL-4, and transforming growth factor (TGF)-β, were quantified using enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (PCR). Phosphorylated p38, JNK, ERK1/2, and NF-κB p65 were also quantified by ELISA, and TRAF6 and IRAK1 mRNA and protein levels were assessed to evaluate inflammatory signaling pathways. In the gingival tissue and systemic circulation, the proinflammatory cytokines IL-1β, IL-8, TNF-α, and IL-6 were significantly downregulated, while the levels of the anti-inflammatory mediators IL-10, IL-4, and TGF-β were significantly increased in the miR-146a-EV group when compared with the control group. miR-146a-EV treatment significantly reduced MAPK and NF-κB activation while downregulating TRAF6 and IRAK1 expression in gingival tissues.</p><p><strong>Conclusion: </strong>miR-146a-transduced MSC-derived EVs ameliorated ligature-induced periodontitis by modulating local and systemic cytokine expression. These results indicate that miR-146a-EVs can be a novel, cell-free therapy for the treatment of periodontitis.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863587","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":"SIRT1-mediated deacetylation of DRP1 suppresses excessive mitophagy and ameliorates pediatric functional dyspepsia.","authors":"Shuan Yin, Dongdong Dai, Gaoyan Wang, Shaomei Zhou","doi":"10.1186/s12865-026-00842-8","DOIUrl":"10.1186/s12865-026-00842-8","url":null,"abstract":"<p><p>Functional dyspepsia (FD) is a prevalent gastrointestinal disorder in children, but its underlying molecular mechanisms remain poorly understood. Mitochondrial dysfunction and excessive mitophagy have been implicated in FD, but the underlying mechanisms remain poorly understood. This study aimed to investigate the role of SIRT1 in mitochondrial quality control and its potential therapeutic value in pediatric FD. Serum samples from pediatric FD patients and healthy controls were analyzed for SIRT1 expression and inflammatory cytokines. Human gastric smooth muscle cells (HGSMCs) were treated with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) to induce mitochondrial stress. Mitochondrial function, mitophagy, oxidative stress, and protein interactions were assessed using qPCR, Western blot, co-immunopcipitation, and functional assays including ATP levels, mitochondrial membrane potential, ROS, MDA, SOD, and GSH-Px. The results showed that SIRT1 was significantly downregulated in both pediatric FD patient sera and CCCP-stimulated HGSMCs, accompanied by elevated pro-inflammatory cytokines including IL-6, TNF-α, and IL-1β. Overexpression of SIRT1 improved cell viability, ATP production, mitochondrial membrane potential, and suppressed excessive mitophagy and oxidative stress. Conversely, DRP1 knockdown phenocopied the protective effects of SIRT1, reducing mitophagy and oxidative stress in CCCP-stimulated cells. SIRT1 directly interacted with DRP1 and promoted its deacetylation at lysine 283, leading to accelerated DRP1 degradation. Rescue experiments confirmed that DRP1 overexpression reversed the protective effects of SIRT1 on mitochondrial function and redox homeostasis. In conclusion, SIRT1 exerts protective effects in pediatric FD by deacetylating DRP1 at K283, thereby inhibiting excessive mitophagy and ameliorating mitochondrial dysfunction and oxidative stress. These findings identify the SIRT1-DRP1 axis as a potential therapeutic target for pediatric FD.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13366741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855882","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":"Elevated serum TNF-α in patients with immune-mediated necrotizing myopathy correlates with muscle damage.","authors":"Xingyu Han, Huizhen Ge, Qing Zhang, Mengge Yang, Bitao Bu","doi":"10.1186/s12865-026-00834-8","DOIUrl":"10.1186/s12865-026-00834-8","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate serum levels of tumor necrosis factor-alpha (TNF-α) in patients with immune-mediated necrotizing myopathy (IMNM) and to explore its correlation with disease activity.</p><p><strong>Methods: </strong>Serum TNF-α levels were measured using an enzyme-linked immunosorbent assay (ELISA). TNF-α mRNA expression in muscle tissues from IMNM patients was detected by reverse transcription quantitative real-time PCR (RT-qPCR). In vitro experiments were performed on human muscle cells stimulated with TNF-α to assess cell viability and the expression of downstream molecules.</p><p><strong>Results: </strong>Serum TNF-α levels were significantly elevated in IMNM patients compared to healthy controls (p = 0.0002). In IMNM patients, TNF-α levels showed a significant positive correlation with serum creatine kinase (CK; p = 0.0004) and lactate dehydrogenase (LDH; p = 0.0137). TNF-α mRNA was also overexpressed in muscle biopsies from patients with IMNM. In vitro, TNF-α stimulation significantly reduced muscle cell viability and upregulated the mRNA expression of downstream inflammatory mediators, including IP-10, MCP-1, IL-6, and phosphorylated p65.</p><p><strong>Conclusion: </strong>Elevated serum TNF-α in IMNM patients is associated with muscle damage and may contribute to disease pathogenesis by amplifying the inflammatory response. These findings suggest that TNF-α could serve as a potential biomarker for assessing disease severity in IMNM.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13361582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833362","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":"The diagnostic and prognostic value of miR-200b on severe pneumonia.","authors":"Shuying Zheng, Xiaopei Zhou, Changhao Cheng","doi":"10.1186/s12865-026-00836-6","DOIUrl":"10.1186/s12865-026-00836-6","url":null,"abstract":"<p><strong>Background: </strong>Severe pneumonia (SP) is a critical infectious disease characterized by excessive inflammatory responses, and the molecular mechanisms underlying its progression remain incompletely understood.</p><p><strong>Objective: </strong>To investigate the expression pattern, diagnostic value, and potential functional regulatory mechanisms of miR-200b in SP.</p><p><strong>Methods: </strong>RT-qPCR was used to detect miR-200b expression levels; ROC curve analysis was used to evaluate its diagnostic performance; prognostic indicators of miR-200b were compared between high- and low-expression groups, and Cox regression was employed to identify independent prognostic factors. In vitro validation of the pro-inflammatory effects of miR-200b. Target genes were identified through Venn diagram-based prediction and dual luciferase reporter assays. Functional recovery experiments were conducted to elucidate regulatory pathways.</p><p><strong>Result: </strong>miR-200b expression was significantly higher in SP patients than in CP/HC groups, with an ROC curve AUC of 0.848 distinguishing SP from CP/HC, demonstrating good diagnostic performance. Elevated miR-200b expression significantly correlated with poorer prognostic indicators and served as an independent risk factor for adverse SP outcomes. In vitro experiments demonstrated that miR-200b expression was upregulated in a concentration- and time-dependent manner following LPS stimulation, promoting IL-6 and TNF-α secretion. RHOA was identified as a direct target gene of miR-200b, and miR-200b exerts pro-inflammatory effects by inhibiting RHOA and activating the NF-κB pathway.</p><p><strong>Conclusion: </strong>miR-200b serves as a potential diagnostic and prognostic biomarker for SP. By targeting RHOA to activate the NF-κB pathway, it promotes inflammatory damage in SP, thus providing a novel therapeutic target for clinical intervention.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13359929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833407","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":"Prognostic significance of inflammatory cytokine polymorphisms in AML: a study of IFNG, TNFA, and IL1B polymorphisms.","authors":"Tsatsralgerel Munkh-Erdene, Takayuki Saitoh, Miri Kitamura, Asumi Kojima, Takafumi Okawa, Tsukasa Oda, Eiji Miyauchi, Nobuo Sasaki, Ikuko Matsumura, Akira Matsumoto, Hisashi Takei, Nobuhiko Kobayashi, Yuri Miyazawa, Yoshiyuki Ogawa, Hiroshi Handa, Nanami Gotoh","doi":"10.1186/s12865-026-00837-5","DOIUrl":"10.1186/s12865-026-00837-5","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory cytokines influence the pathogenesis and progression of acute myeloid leukaemia (AML), not only by shaping the leukemic microenvironment, but also by supporting leukaemia stem cell survival and resistance to therapy. We, therefore, investigated the associations between the cytokine polymorphisms IFNG+874 A/T, TNFA-857 C/T, and IL1B -31 C/T and AML outcomes, as well as their influence on clinical features.</p><p><strong>Results: </strong>Ninety-three patients with AML and 117 healthy controls were analysed. The T allele of TNFA - 857 C/T (i.e., the high-expression allele) was observed at a significantly higher frequency in the patients with AML vs. the controls (AML vs. control = 24.7% vs. 16.2%, p = 0.04). Patients with the high-expression TT genotype had shorter overall survival (TT vs. CC = 46.0 vs. 224.1 months, p < 0.001). Patients with the high-expression non-CC genotype relapsed more frequently than those with the low-expression CC genotype (relapse vs. non-relapse = 55.8% vs. 26.9%, p = 0.01). No significant associations were observed for the IFNG + 874 A/T and IL1B -31 C/T polymorphism.</p><p><strong>Conclusion: </strong>TNFA - 857 C/T polymorphisms can influence patient susceptibility to AML, as well as its prognosis. This suggests a link between chronic inflammation and leukemogenesis, as well as the potential value of TNFA genotyping in risk assessments.</p>","PeriodicalId":9040,"journal":{"name":"BMC Immunology","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13361117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811103","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}