Central European Journal of Immunology最新文献

{"title":"Glutaminase 1-mediated glutaminolysis regulates tuberculosis progression by modulating Th1 and Th17 immune responses.","authors":"Xiaozhen Cai, Yidan Huang, Lili Zeng, Rong Rong","doi":"10.5114/ceji/208684","DOIUrl":"10.5114/ceji/208684","url":null,"abstract":"<p><strong>Introduction: </strong>Mycobacterium tuberculosis-mediated tuberculosis (TB) is an infectious disease that results in approximately 1.2 million deaths annually. Glutaminase (GLS1) is a metabolic enzyme involved in glutaminolysis. The current study examined the roles and mechanisms of GLS1 in TB progression.</p><p><strong>Material and methods: </strong>Peripheral blood mononuclear cells (PBMCs) were extracted from TB patients and healthy individuals, and CD4⁺ T and CD14⁺ monocytes were sorted. PBMCs were incubated with M. tuberculosis strain H37Rv lysate to stimulate immune responses and treated with BPTES, a GLS1 inhibitor. RT-qPCR and western blotting were employed to detect mRNA and protein levels, respectively. Immunophenotyping of cells was performed using flow cytometry. ELISA was used to determine cytokine levels. Colony-forming unit assays were used to evaluate M. tuberculosis survival in macrophages. ChIP assays were used to detect the enrichment of H3K9ac/H3K27ac at the gene promoters.</p><p><strong>Results: </strong>GLS1 was elevated in CD4⁺ T cells from TB patients and H37Rv lysate-stimulated PBMCs. GLS1-mediated glutaminolysis promoted Th1 and Th17 cell differentiation. Inhibition of GLS1 by BPTES facilitated M. tuberculosis survival in macrophages. GLS1 inhibition reduced H3K9ac and H3K27ac epigenetic modification in the promoter region of interferon <i>γ</i> and interleukin 17.</p><p><strong>Conclusions: </strong>GLS1-mediated glutaminolysis may regulate TB progression by modulating Th1 and Th17 immune responses via epigenetic regulation.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"121-132"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863576","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":"Uncovering common pathways and potential drug targets in COVID-19 and venous thrombosis <i>via</i> systems biology approaches.","authors":"Boyang Yu, Rongjian Gao, Wenchao Ma","doi":"10.5114/ceji/201957","DOIUrl":"10.5114/ceji/201957","url":null,"abstract":"<p><strong>Introduction: </strong>COVID-19 and venous thrombosis pose significant global health challenges. Recent studies suggest a potential overlap in their underlying molecular mechanisms, particularly immune responses and inflammation. This study aims to elucidate shared molecular pathways between COVID-19 and venous thrombosis, identify common biomarkers, and propose potential therapeutic targets through a comprehensive multi-dataset analysis.</p><p><strong>Material and methods: </strong>Public datasets (GSE171110, GSE189990, GSE178246, GSE48000, and GSE19151) were analyzed using the \"Limma\" package in R for differential gene expression analysis. Functional enrichment (GO, KEGG) was conducted via the \"ClusterProfiler\" package. Protein-protein interaction (PPI) networks, transcription factor (TF)-target, and miRNA-target networks were constructed using TRRUST and miRDB databases. Drug sensitivity was assessed using CellMiner, and feature genes were identified using LASSO regression. Immune infiltration analysis was performed with CIBERSORT, and key genes were validated using qRT-PCR and animal models.</p><p><strong>Results: </strong>Key differentially expressed genes (DEGs), including SELP and CLEC4D, were identified, highlighting their roles in immune regulation and thrombosis. Drug sensitivity analysis revealed correlations with specific chemotherapeutic agents. Immune infiltration analysis demonstrated increased expression of SELP and CLEC4D in certain immune cells, confirmed by qRT-PCR and in animal models.</p><p><strong>Conclusions: </strong>This study uncovered shared molecular mechanisms between COVID-19 and venous thrombosis, identifying potential biomarkers and therapeutic targets such as SELP and CLEC4D. These findings provide new insights into the diagnosis and treatment of both conditions.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"197-222"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863600","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":"B cells, autoimmunity, and innate immunity in 22q11.2 deletion syndrome: a two-center study and review of the literature.","authors":"Ezgi Topyildiz, Selime Ozen Boluk, Ilke Baş, Emine Ulgen, Nesrin Gulez, Neslihan Edeer Karaca, Ferah Genel, Guzide Aksu, Necil Kutukculer","doi":"10.5114/ceji/208683","DOIUrl":"10.5114/ceji/208683","url":null,"abstract":"<p><strong>Introduction: </strong>A few studies have reported that 22q11.2 del syndrome (DiGeorge syndrome - DGS) is associated with alterations in B-lymphocytes and innate immunity that predispose to infections and autoimmunity. The present study investigated the B-cell compartment, autoimmunity markers, and components of innate immunity, including NK cells, NK-specific cytotoxicity, phagocytic functions, and adhesion molecules.</p><p><strong>Material and methods: </strong>Thirty-five DGS patients and twenty healthy controls were evaluated. Nephelometric, flow cytometric, ELISA and immunofluorescence techniques were used.</p><p><strong>Results: </strong>There was no significant difference between the study and control groups regarding gender and age. Serum IgG, IgM levels and percentages, and antibodies against vaccine antigens were significantly lower in DGS patients. In DGS patients, 57.2% had low levels of non-switched memory B-cells, and 22.8% had low values of switched memory B-cells. Immature transitional B-cells, immature B-cells, plasmablasts, and active B-cells were significantly elevated. Autoantibodies were found positive in between 2.9% and 14.3% in the patient group. Natural killer T (NKT) cells and regulatory T cells (Tregs) were significantly decreased, whereas Fas⁺ active cytotoxic cells and Fas⁺ naive T helper cells were significantly elevated in DGS patients. NK-specific cytotoxicity was found to be higher in the patient group.</p><p><strong>Conclusions: </strong>Defects in humoral immunity, including immunoglobulin deficiencies and decreases in class-switched and nonclass-switched memory B-cell compartments, were common in DGS patients. While decreased Treg and NKT cells play a role in the increased incidence of autoimmunity, increased Fas⁺ cells counteract autoimmunity. Based on all these data, we would like to emphasize the importance of monitoring DGS patients for immune dysregulation.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"184-196"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863608","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":"Correlation between double-stranded DNA and rheumatoid arthritis.","authors":"Mingwei Lv, Yirui Wang, Juan Du, Jingyue Wang, Zhuo Li, Yang Han, Xinyu Feng, Xiaofen Guo, Haoran Shen, Yuge Wang, Guanglei Shi, Yuhang Liu, Weiwei Chen, Qi Zhen, Ruimin Wang, Liangdan Sun","doi":"10.5114/ceji/203824","DOIUrl":"10.5114/ceji/203824","url":null,"abstract":"<p><strong>Introduction: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disease influenced by environmental factors. Double-stranded DNA (dsDNA) serves as an antigen in various autoimmune diseases and is affected by meteorological factors. However, the relationships among the circulating dsDNA level, RA inflammatory immune mechanisms, and seasonal meteorological factors remain unclear.</p><p><strong>Material and methods: </strong>Serum dsDNA levels were measured in patients with RA and healthy controls, and correlations with archived data on seasonal meteorological changes were examined. Quantitative PCR was performed to assess the gene expression of relevant receptor markers in the peripheral circulation of patients and controls.</p><p><strong>Results: </strong>The mean serum dsDNA level was significantly higher in patients with RA than in controls (1.16 ±0.36 ng/ml vs. 0.92 ±0.20 ng/ml, p < 0.001). The expression of genes related to dsDNA receptors, single-stranded RNA receptors, dsRNA receptors, ALR inflammasome-associated inflammatory factors, interferon (IFN) <i>α</i>1, IFN <i>β</i>1, and low-density lipoprotein was upregulated in patients with RA.</p><p><strong>Conclusions: </strong>dsDNA levels in the peripheral circulation of patients with RA are elevated and affected by seasonal climatic factors. This elevation enhances the expression of ALR inflammasome-related inflammatory factors and type I IFN. These findings provide a foundation for future investigations into the mechanisms underlying the link between climate variability and RA progression.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"70-83"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162071","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":"HE4: a potential diagnostic biomarker in autoimmune diseases.","authors":"Qinni Yang","doi":"10.5114/ceji/208686","DOIUrl":"10.5114/ceji/208686","url":null,"abstract":"<p><p>Human epididymal protein 4 (HE4), also known as protein four-disulfide core domain 2, is a secretory protein that is highly expressed in epithelial ovarian cancer. HE4 has higher specificity and sensitivity than traditional biomarkers in ovarian cancer, making it an effective marker for monitoring the progression of ovarian cancer. Given the similarities between the pathological processes in cancer and autoimmune diseases (ADs), namely overactivation of immune cells and involvement of inflammatory responses, patients with ADs may have an increased risk of cancer. Accumulating evidence suggests that HE4 is strongly associated with ADs such as systemic lupus erythematosus, Sjögren's syndrome, rheumatoid arthritis-associated interstitial lung disease, and immunoglobulin A nephropathy. Several studies have reported that HE4 reflects disease severity and has excellent potential as a biomarker for the diagnosis and progression monitoring of ADs. In this article, we provide a detailed overview of the research on the biological function of HE4 in ADs and provide insights into whether HE4 has the potential to serve as a candidate biomarker for chronic inflammatory ADs.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"111-120"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863568","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":"Musculin enhances the immune function of peritoneal macrophages in mice.","authors":"Yu Xia, Xin Zhang, Jing Yu, Guochang Liu, Daiqi Chen, Lu Kang, Yun Wang, Jun Yan","doi":"10.5114/ceji/205378","DOIUrl":"10.5114/ceji/205378","url":null,"abstract":"<p><strong>Introduction: </strong>Macrophages play a key role in infection, and musculin (MSC) is closely associated with immune cells. The objective of this study was to investigate the effect of MSC on the immune function of mouse peritoneal macrophages.</p><p><strong>Material and methods: </strong>Peritoneal macrophages from wild-type (WT) and MSC knockout (MSC-/-) mice were obtained and cultured for 12 hours. The cells were subsequently treated with lipopolysaccharide (LPS). After 24 hours, the peritoneal macrophages and their supernatants were collected. The changes in the adhesion index in each group were then recorded by cell counting, and the phagocytic index and phagocytic rate were calculated via bacterial phagocytosis experiments. Additionally, the levels of interleukin (IL)-1 <i>β</i>, IL-6, IL-10 and tumour necrosis factor <i>α</i> (TNF-<i>α</i>) in the cell supernatant were measured via enzyme-linked immunosorbent assay (ELISA). The ratios of cluster of differentiation (CD) 16/32 and CD206 were analysed via flow cytometry.</p><p><strong>Results: </strong>At 24 hours after LPS treatment, the number of peritoneal macrophages in the MSC-/- group was lower than that in the WT group, while the adhesion index in the former group was higher than that in the latter group. Compared with those in the WT group, the phagocytosis index and phagocytosis rate were significantly lower in the MSC-/- group, while the levels of IL-1 <i>β</i>, IL-6, and TNF-<i>α</i> were higher, and the level of IL-10 was lower. In addition, the number of type 2 (M2) macrophages was lower in the same comparison.</p><p><strong>Conclusions: </strong>Musculin may enhance the immune function of peritoneal macrophages in mice.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 2","pages":"158-166"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863650","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":"Lactylated chitinase-3-like protein 1 promotes the development of sepsis.","authors":"Shiliang Wei, Xin Wang, Hailong Yan, Xian Wang, Binjian Yang","doi":"10.5114/ceji/204065","DOIUrl":"10.5114/ceji/204065","url":null,"abstract":"<p><p>Chitinase-3-like protein 1 (CHI3L1) is overexpressed in various types of diseases, particularly in sepsis, and contributes to disease progression. However, the role of CHI3L1 and the pathways involved in the progression of sepsis are not yet completely understood. In the present study, lipopolysaccharide (LPS) was used to construct mouse and cell models of sepsis. Reverse transcription-quantitative PCR was used to detect the expression of CHI3L1. Cycloheximide was used to analyze the protein stability of CHI3L1. The mRNA levels of CHI3L1 and the lactate content were found to be significantly elevated in the serum of patients with sepsis and in LPS-exposed RAW264.7 cells. Furthermore, LPS exposure significantly increased the lactylation of CHI3L1 in RAW264.7 cells. Lactate treatment promoted the lactylation of CHI3L1 and 2-DG treatment inhibited it. Lactylation induced the degradation of CHI3L1 protein. Furthermore, CHI3L1 knockdown inhibited macrophage apoptosis and the release of inflammatory cytokines (IL-1 <i>β</i>, IL-6 and TNF-<i>α</i>) and inactivated the NF-<i>κ</i>B pathway in the LPS-exposed RAW264.7 cells. In addition, the analysis of the mouse model of sepsis revealed that knockdown of CHI3L1 reduced the IL-1 <i>β</i>, IL-6, TNF-<i>α</i>, creatinine, blood urea nitrogen, alanine transaminase, and aspartate aminotransferase levels, and attenuated damage induced by sepsis to the heart, liver, lung, and kidneys in mice with sepsis. On the whole, the present study demonstrates that the lactylation modification of CHI3L1 promotes the development of sepsis. Thus, focusing on CHI3L1 expression changes may prove to be a promising approach for the treatment of sepsis in the future.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"51-62"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162041","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":"RAB40C regulates SNX9 stability <i>via</i> the ubiquitin-proteasome system and modulates the Hippo signaling pathway of prostate adenocarcinoma.","authors":"Liang Qin, Ning Yang, Fan Yang, Xuwei Lu, Jiawen Wu, Zhuifeng Guo","doi":"10.5114/ceji.2025.156367","DOIUrl":"10.5114/ceji.2025.156367","url":null,"abstract":"<p><strong>Introduction: </strong>Aim of the study was to investigate the roles and interaction mechanisms of RAB40C and SNX9 in prostate adenocarcinoma (PRAD) progression and their impact on the Hippo signaling pathway. PRAD is a significant health concern, and understanding the molecular underpinnings is essential for its effective management. Objective of this study was to identify key genes and pathways involved in PRAD using weighted gene co-expression network analysis (WGCNA) and determine the functional implications of RAB40C and its relationship with SNX9.</p><p><strong>Material and methods: </strong>WGCNA was used to chart gene co-expression patterns in PRAD. Functional enrichment analyses of significant modules were performed, and prognostic insights were derived through differential gene expression analysis. The interaction between RAB40C and SNX9 was elucidated using various in vitro assays and databases.</p><p><strong>Results: </strong>WGCNA identified a module (MEblue) highly correlated with PRAD. The hub gene was revealed, with RAB40C being central to PRAD progression. The knockdown of RAB40C inhibited PRAD cell proliferation, migration, and invasion. SNX9 was identified as a substrate protein interacting with RAB40C. The silencing of RAB40C led to increased SNX9 expression, suggesting an inverse regulatory relationship. RAB40C promoted SNX9 degradation via the ubiquitin-proteasome pathway. Silencing RAB40C reduced PRAD cell proliferation, migration, and invasion, effects that were counteracted by simultaneous SNX9 suppression. The interaction between RAB40C and SNX9 influenced target proteins of the Hippo signaling pathway.</p><p><strong>Conclusions: </strong>RAB40C is essential for the progression of PRAD, partly through modulating SNX9 levels and the Hippo signaling pathway. This interplay offers novel insights for PRAD therapeutic strategies.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"31-50"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161744","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":"A rare case of sporotrichosis in a patient with late latent syphilis and diabetes mellitus: immunological aspects of sporotrichosis.","authors":"Natalia A Welc, Aleksandra Anioła, Sandra Ważniewicz, Honorata Kubisiak-Rzepczyk, Monika Bowszyc-Dmochowska, Adriana Polańska, Ryszard Żaba, Aleksandra Dańczak-Pazdrowska","doi":"10.5114/ceji/203825","DOIUrl":"10.5114/ceji/203825","url":null,"abstract":"<p><p>Sporotrichosis, caused by Sporothrix schenckii, typically infects humans through skin trauma, leading to nodules or ulcers that complicate diagnosis. Rare forms, such as disseminated cutaneous sporotrichosis, occur more often in immunosuppressed patients or those with diabetes or alcohol use disorder. We report a 49-year-old male patient with type 2 diabetes mellitus who developed painful ulcerations on his lower limbs following a cat scratch. A deep tissue biopsy confirmed mycelial hyphae, and culture identified Sporothrix spp. A biopsy from a left thigh lesion revealed syphilitic exanthem findings. Treponema pallidum antibodies were positive, with a TPHA titer of 1 : 320. The patient was diagnosed with sporotrichosis and late latent syphilis, treated with benzathine penicillin for syphilis and itraconazole for sporotrichosis, resulting in significant improvement after two months. This case underscores the importance of mycological diagnostics - deep tissue biopsy, culture, and histopathological analysis - in distinguishing sporotrichosis from similar conditions, especially in immunocompromised patients with unresponsive lesions.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"51 1","pages":"63-69"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162125","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":"Curcumin modulates inflammatory responses in peripheral blood mononuclear cells from women with gestational diabetes mellitus.","authors":"Zhenzhen Liu, Liu Zheng, Yao Wu, Huijuan Li, Junfang Liu","doi":"10.5114/ceji.2025.153886","DOIUrl":"10.5114/ceji.2025.153886","url":null,"abstract":"<p><strong>Introduction: </strong>Curcumin is a multi-functional component with anti-inflammatory and immunomodulatory properties. Unregulated immune responses may be a causative factor in the development of gestational diabetes mellitus (GDM). This study investigated the effect and mechanisms of curcumin on regulatory T cells/Th17 axis, and secretion of related cytokines (interleukin [IL]-17A, IL-6, and IL-10) in peripheral blood mononuclear cells (PBMCs) of healthy women and women with GDM.</p><p><strong>Material and methods: </strong>This research involved in vitro experiments to evaluate the influence of curcumin on PBMCs; none of the subjects were taking any curcumin supplementation. Flow cytometry and ELISA were used in this study. Curcumin (1 μM, for 72 hours) treatment reduced the frequency of Th17 cells and the levels of related cytokines (IL-6, and IL-17) in women with GDM.</p><p><strong>Results: </strong>The percentage of Th17 cells decreased after treatment with curcumin relative to untreated cells in the GDM group (p = 0.04). Curcumin reduced the IL-17A level in the GDM group (p = 0.01). Curcumin treatment reduced the IL-6 level only in the GDM group (p = 0.02). In the presence of curcumin, the IL-10 level in the supernatants of cell culture was significantly higher in the GDM group compared to the negative control (p = 0.0008).</p><p><strong>Conclusions: </strong>The findings of the present study showed that curcumin modulated the immune responses via balancing of Treg/Th17 in women with GDM. Curcumin increased the level of IL-10, an anti-inflammatory cytokine, whereas it decreased the level of IL-6, which is related to the differentiation of Th17 cells. Curcumin treatment decreased the expression of IL-17A, the main secretory cytokine of Th17 cells. In conclusion, curcumin may act as an immunomodulator component in GDM by balancing the Th17/Treg axis.</p>","PeriodicalId":9694,"journal":{"name":"Central European Journal of Immunology","volume":"50 3","pages":"319-327"},"PeriodicalIF":1.6,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12721229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145818286","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}