Archivum Immunologiae et Therapiae Experimentalis最新文献

BDH2 Inhibits Lung Adenocarcinoma Metastasis by Promoting Ferroptosis. BDH2通过促进铁下垂抑制肺腺癌转移。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-04-09 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0012

Qiao Yang, Lin Tian, Xiaodong Chen, Xiong Mei, Yongli Nie, Jun Chen

{"title":"BDH2 Inhibits Lung Adenocarcinoma Metastasis by Promoting Ferroptosis.","authors":"Qiao Yang, Lin Tian, Xiaodong Chen, Xiong Mei, Yongli Nie, Jun Chen","doi":"10.2478/aite-2026-0012","DOIUrl":"https://doi.org/10.2478/aite-2026-0012","url":null,"abstract":"To investigate the role of 3-hydroxybutyrate dehydrogenase 2 (BDH2) in regulating ferroptosis and its impact on the metastasis of lung adenocarcinoma (LUAD). Expression levels of BDH2 were modulated in LUAD cell lines (A549, PC9) using pcDNA-BDH2 plasmid transfection. Cell motility was assessed by Transwell assays, while ferroptosis-associated markers, including Fe2+, malondialdehyde (MDA), lipid reactive oxygen species (ROS), ACSL4, and GPX4, were evaluated by biochemical assays, flow cytometry, and Western blotting. The involvement of the Nrf2/HO-1 signaling axis was analyzed by Western blotting and RT-qPCR. Furthermore, a xenograft mouse model was established to confirm the effect of BDH2 on tumor progression and metastasis in vivo. Overexpression of BDH2 significantly inhibited LUAD cell migration and invasion. BDH2 upregulation enhanced ferroptosis, effects that were reversed by the ferroptosis inhibitor Fer-1. Mechanistically, BDH2 suppressed the activation of the Nrf2/HO-1 pathway, thereby enhancing sensitivity to ferroptosis. In vivo, BDH2 overexpression markedly reduced tumor growth and metastasis in nude mice, while inhibition of ferroptosis attenuated these effects. BDH2 suppresses metastasis in LAUD by promoting ferroptosis via suppression of the Nrf2/HO-1 pathway, highlighting BDH2 as a potential therapeutic target for LUAD.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653404","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

Di-Chimeric Cell Therapy Derived From Hematopoietic and Mesenchymal Stem Cells Promotes Immune Tolerance and Extends Vascularized Composite Allograft Survival. 来自造血干细胞和间充质干细胞的双嵌合细胞治疗促进免疫耐受并延长血管化复合同种异体移植物的存活。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-04-09 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0013

Maria Siemionow, Safak Halil Uygur, Katarzyna Stawarz, Lucile Chambily, Katarzyna Budzynska, Weronika Radecka

{"title":"Di-Chimeric Cell Therapy Derived From Hematopoietic and Mesenchymal Stem Cells Promotes Immune Tolerance and Extends Vascularized Composite Allograft Survival.","authors":"Maria Siemionow, Safak Halil Uygur, Katarzyna Stawarz, Lucile Chambily, Katarzyna Budzynska, Weronika Radecka","doi":"10.2478/aite-2026-0013","DOIUrl":"https://doi.org/10.2478/aite-2026-0013","url":null,"abstract":"Chimerism-based strategies remain promising for tolerance induction in solid organ and vascularized composite allograft (VCA) transplantation. This study aimed to develop a novel, less toxic chimeric cell therapy to prolong allograft survival and reduce the need for lifelong immunosuppression. Di-chimeric cells (DCC) were created via polyethylene glycol (PEG)-mediated ex vivo fusion of allogeneic hematopoietic stem cells (HSC) and mesenchymal stem cells (MSC) derived from August Copenhagen Irish (ACI) and Lewis rats. Twenty-four fully major histocompatibility complex (MHC)-mismatched groin flap VCAs were transplanted from ACI rat major histocompatibility complex (rat MHC) (RT1a) donors to Lewis (RT11) recipients under a 7-day immunosuppressive protocol of anti-αβTCR antibody and tacrolimus, combined with four different cell therapies of n = 6/group: Group 1, saline control; Group 2, MSC; Group 3, HSC/HSC DCC; and Group 4, HSC/MSC DCC. DCC were delivered via the intraosseous injection. DCC phenotype was confirmed by flow cytometry (FC). Graft rejection was evaluated macroscopically. A single DCC dose significantly prolonged VCA survival, with the best results in Group 4 (94 ± 1.65 days), followed by Group 3 (66 ± 1.24 days), Group 2 (45.5 ± 4.08 days), and Group 1 (38 ± 4.29 days). This study confirmed immunomodulatory and tolerogenic properties of DCC, supporting VCA transplantation.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653488","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

Fusobacterium nucleatum Promotes Bladder Cancer Development Through lncRNA IDH1-AS1-Mediated Autophagy. 核梭杆菌通过lncRNA idh1 - as1介导的自噬促进膀胱癌的发展。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-03-31 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0011

JunJie Hu, BiYan Li, XiaoYuan Xu, ShuYing Lin, Shui Xu, YueJun Chen, GaoYin Tong

{"title":"Fusobacterium nucleatum Promotes Bladder Cancer Development Through lncRNA IDH1-AS1-Mediated Autophagy.","authors":"JunJie Hu, BiYan Li, XiaoYuan Xu, ShuYing Lin, Shui Xu, YueJun Chen, GaoYin Tong","doi":"10.2478/aite-2026-0011","DOIUrl":"https://doi.org/10.2478/aite-2026-0011","url":null,"abstract":"Bladder cancer is a prevalent malignancy with a high recurrence rate, necessitating the identification of novel molecular targets for diagnosis and therapy. Recent studies have highlighted the role of long noncoding RNAs (lncRNAs) in cancer progression. This study aims to investigate the role of the lncRNA IDH1-AS1 in bladder cancer, focusing on its effects on tumor growth, cell proliferation, and autophagy-related protein expression. We utilized both in vivo and in vitro models to assess the impact of IDH1-AS1 overexpression and knockdown. Tumor growth was evaluated in nude mice model of bladder cancer, while cell proliferation was measured using the EDU assay. Protein expression levels of Beclin1, P62, and LC3 were determined by Western Blot analysis. Gene expression of IDH1-AS1 was quantified using quantitative polymerase chain reaction (qPCR). Overexpression of IDH1-AS1 in nude mice model of bladder cancer led to a significant increase in tumor volume and weight, whereas knockdown of IDH1-AS1 resulted in a substantial decrease in tumor size. In vitro, IDH1-AS1 overexpression significantly enhanced cell proliferation, while its knockdown reduced proliferation. Western Blot analysis revealed that IDH1-AS1 overexpression increased the levels of autophagy-related proteins Beclin1 and LC3, and decreased P62 protein levels, with contrary effects observed upon IDH1-AS1 knockdown. qPCR confirmed successful modulation of IDH1-AS1 expression in experimental groups. Our findings indicate that IDH1-AS1 promotes tumor growth and cell proliferation in bladder cancer, potentially through the regulation of autophagy-related proteins. These results suggest that IDH1-AS1 could serve as a novel biomarker and therapeutic target for bladder cancer.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760607","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

Bowel-Associated Dermatosis and Arthritis Syndrome (BADAS) - A Literature Review With Diagnostic and Therapeutic Implications and a Report of Two Cases of BADAS Associated With Inflammatory Bowel Disease. 肠相关皮肤病和关节炎综合征（BADAS）——具有诊断和治疗意义的文献综述和两例BADAS合并炎症性肠病的报告。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-02-21 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0010

Raman Nitskovich, Aleksandra Jóźwik, Piotr Sobolewski, Paweł Głuszak, Dagmara S Mahadea, Irena Walecka

{"title":"Bowel-Associated Dermatosis and Arthritis Syndrome (BADAS) - A Literature Review With Diagnostic and Therapeutic Implications and a Report of Two Cases of BADAS Associated With Inflammatory Bowel Disease.","authors":"Raman Nitskovich, Aleksandra Jóźwik, Piotr Sobolewski, Paweł Głuszak, Dagmara S Mahadea, Irena Walecka","doi":"10.2478/aite-2026-0010","DOIUrl":"https://doi.org/10.2478/aite-2026-0010","url":null,"abstract":"Bowel-associated dermatosis-arthritis syndrome (BADAS) is a rare neutrophilic dermatosis characterized by recurrent erythematous macules, papules or vesicopustules accompanied by fever, malaise, arthralgia and peripheral arthritis. Although originally described after intestinal bypass procedures, BA-DAS is increasingly recognized in inflammatory bowel disease (IBD), yet remains underdiagnosed and lacks practical guidance. We reviewed published IBD-associated BADAS cases to define clinical patterns and therapeutic options, and report two additional cases managed by an interdisciplinary team. Across the literature, 21 IBD-associated BADAS cases were identified, with a female predominance (65%) and a mean age at onset of 36.7 years; pediatric presentations accounted for 17%. Ulcerative colitis (12 cases) and Crohn's disease (10 cases) were the most frequent underlying conditions. BADAS was often diagnosed concurrently with IBD, indicating that the combination of cutaneous eruptions, joint inflammation and systemic symptoms should prompt gastrointestinal evaluation. Frequently reported abnormalities included leukocytosis, anemia and elevated inflammatory markers, and skin histopathology typically showed a neutrophilic dermatosis often with leukocytoclastic vasculitis. Case 1 (30-year-old woman with ulcerative colitis) achieved sustained remission with antibiotics, corticosteroid taper, cyclosporine induction and azathioprine maintenance. Case 2 (67-year-old man with Crohn's disease) responded to antibiotics followed by infliximab, with resolution of skin, joint and intestinal activity. We propose a pragmatic management approach integrating antibiotics, optimization of IBD therapy and early use of biologics (preferably anti-TNF) in severe or steroid-refractory disease.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"74 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146776118","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

Mechanism of RBM15 in Regulating PD-L1-Mediated Immune Escape in Ovarian Cancer Through the JAK2/STAT3/STAT5 Pathway. RBM15通过JAK2/STAT3/STAT5途径调控pd - l1介导的卵巢癌免疫逃逸的机制

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-02-11 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0009

Chengju Zhang, Tiantian Feng, Hu Wang, Deng He, Xi Wang, Shangqi Ni, Yuesong Wang

引用次数: 0

Neuronal Transdifferentiation in Humans: Protocols for Monocytes Conversion into Neuronal-Like Cells with Small Molecules. 人类神经元转分化：单核细胞转化为具有小分子的神经元样细胞的方案。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2026-01-26 eCollection Date: 2026-01-01 DOI: 10.2478/aite-2026-0008

Kornelia Jankowska, Saeid Ghavami, Jolanta Hybiak, Marek J Łos

引用次数: 0

Significance of the LL-37 Peptide Delivered from Human Cathelicidin in the Pathogenesis, Treatment, and Diagnosis of Sepsis. 人抗菌肽传递LL-37肽在脓毒症发病、治疗和诊断中的意义

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2025-09-07 eCollection Date: 2025-01-01 DOI: 10.2478/aite-2025-0025

Angelika Mańkowska, Paulina Paprocka, Grzegorz Król, Agata Lesiak, Jakub Spałek, Ewelina Piktel, Sławomir Okła, Piotr Bijak, Wiesława Niklińska, Bonita Durnaś, Robert Bucki

{"title":"Significance of the LL-37 Peptide Delivered from Human Cathelicidin in the Pathogenesis, Treatment, and Diagnosis of Sepsis.","authors":"Angelika Mańkowska, Paulina Paprocka, Grzegorz Król, Agata Lesiak, Jakub Spałek, Ewelina Piktel, Sławomir Okła, Piotr Bijak, Wiesława Niklińska, Bonita Durnaś, Robert Bucki","doi":"10.2478/aite-2025-0025","DOIUrl":"https://doi.org/10.2478/aite-2025-0025","url":null,"abstract":"Antimicrobial peptides, which function as the first line of host immune defense, have recently been identified as important immunomodulators of inflammation, and are involved as regulatory molecules in infections, including sepsis. Treatment of sepsis is very complex and remains largely challenging and sometimes ineffective. This creates a need to develop new therapeutic strategies focusing not only on the elimination of sepsis-causing microorganisms, which can be achieved with antibiotics, but also on the control of the immune system and its overactive response resulting in increased vascular endothelial permeability. One approach to develop new treatments for patients with sepsis is to better understand the pleiotropic function of the human LL-37 peptide that originates from the human cathelicidin antibacterial protein (h-CAP18). An increasing number of studies indicate high dynamics of changes in LL-37 concentration in the blood during sepsis. Additionally, in animal models, administration of exogenous LL-37 peptide to mice with experimentally induced sepsis increases their survival. It can therefore be assumed that knowledge of the molecular mechanism of cathelicidin LL-37 action, as well as the synthesis of its stable analogs, will result in progress in the diagnosis and therapy of sepsis.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"73 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145074226","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

From Fleas to T Lymphocytes and Beyond: How did I Become an Immunologist, and What Has Resulted from It? 从跳蚤到T淋巴细胞及其他：我是如何成为一名免疫学家的，以及它带来了什么？

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.2478/aite-2025-0024

Paweł Kisielow

引用次数: 0

Overexpression of Annexin A1 Inhibits Pyroptosis and Improves Dry Eye Signs by Regulating the TRIM72/Nrf2/HO-1 Signaling Pathway. 膜联蛋白A1过表达通过调节TRIM72/Nrf2/HO-1信号通路抑制焦亡，改善干眼体征。

IF 3.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2025-08-06 eCollection Date: 2025-01-01 DOI: 10.2478/aite-2025-0022

Li Zhang, Peng Chen, Pengfei Han, Huizhe Fu, Bin Sun

{"title":"Overexpression of Annexin A1 Inhibits Pyroptosis and Improves Dry Eye Signs by Regulating the TRIM72/Nrf2/HO-1 Signaling Pathway.","authors":"Li Zhang, Peng Chen, Pengfei Han, Huizhe Fu, Bin Sun","doi":"10.2478/aite-2025-0022","DOIUrl":"10.2478/aite-2025-0022","url":null,"abstract":"This study aimed to investigate the therapeutic potential of annexin A1 (ANXA1) overexpression in improving the signs of dry eye disease (DED) and to elucidate the underlying molecular mechanism. A murine model of DED was established by topical application of 0.2% benzalkonium chloride (BAC), and human corneal epithelial (HCE-T) cells were exposed to 0.0005% BAC for in vitro experiments. ANXA1 was overexpressed using adenoviral vectors, and the effects on tear production, pyroptosis, and activation of the tripartite motif-containing protein 72 (TRIM72)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway were evaluated using Western blotting, Schirmer test, Terminal deoxynucleotidyl Transferase dUTP Nick End Labeling (TUNEL) assays, and fluorescent probe analyses. To further examine the role of TRIM72, its expression was silenced with specific small interfering RNA (siRNA), and the consequent impact on ANXA1-mediated therapeutic effects was assessed. ANXA1 expression was significantly reduced in both in vivo and in vitro DED models. Restoration of ANXA1 through overexpression significantly improved tear secretion and suppressed pyroptosis in the murine model. Similarly, in HCE-T cells, ANXA1 overexpression not only enhanced cellular proliferation but also significantly inhibited pyroptosis. Mechanistic investigations demonstrated that ANXA1 overexpression activated the TRIM72/Nrf2/HO-1 signaling pathway by increasing TRIM72, Nrf2, and HO-1 expression. Notably, silencing TRIM72 abolished the therapeutic effects of ANXA1 overexpression, thereby confirming that activation of this pathway is essential for mediating the protective effects of ANXA1 against DED. Overexpression of ANXA1 inhibits pyroptosis and improves dry eye signs by regulating the TRIM72/Nrf2/HO-1 axis.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"73 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788152","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

Knockdown of MBD2 Attenuates LPS-Stimulated Inflammation and Apoptosis in WI-38 Cells Through the STAT-3 Pathway. MBD2的下调通过STAT-3途径减弱lps刺激的WI-38细胞的炎症和凋亡。

IF 2.9 4区医学

Archivum Immunologiae et Therapiae Experimentalis Pub Date : 2025-07-19 eCollection Date: 2025-01-01 DOI: 10.2478/aite-2025-0021

Yao Chen, Liqun Lu

{"title":"Knockdown of MBD2 Attenuates LPS-Stimulated Inflammation and Apoptosis in WI-38 Cells Through the STAT-3 Pathway.","authors":"Yao Chen, Liqun Lu","doi":"10.2478/aite-2025-0021","DOIUrl":"https://doi.org/10.2478/aite-2025-0021","url":null,"abstract":"This study aims to investigate the role of MBD protein 2 (MBD2) in the pneumonia cell model of lipopolysaccharide (LPS)-stimulated WI-38 cells and to uncover the mechanism. LPS-stimulated WI-38 cells were constructed as an in vitro pneumonia model. Quantitative polymerase chain reaction (qPCR) and immunoblot assays showed MBD2 expression in WI-38 cells. Cell counting kit-8 (CCK-8) assays showed the growth of WI-38 cells. Flow cytometry assays showed the apoptosis of WI-38 cells after LPS treatment and siRNA transfection. Enzyme-linked immunosorbent assay (ELISA) and qPCR assays showed the effects on inflammation, and immunoblot assays further confirm the mechanism. MBD2 was highly expressed in LPS-stimulated WI-38 cells. Knockdown of MBD2 alleviates production of cellular inflammatory cytokines in LPS-stimulated WI-38 cells. Further, knockdown of MBD2 alleviates apoptosis in LPS-stimulated WI-38 cells. Mechanically, the knockdown of MBD2 regulates the signal transducer and activator of transcription (STAT)-3 pathway in LPS-stimulated WI-38 cells. Knockdown of MBD2 attenuates LPS-stimulated inflammation and apoptosis in WI-38 cells through the STAT-3 pathway. Therefore, MBD2 could serve as a promising target of pediatric pneumonia.","PeriodicalId":8389,"journal":{"name":"Archivum Immunologiae et Therapiae Experimentalis","volume":"73 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666964","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