Immunological Investigations最新文献_第8页

Describing Elephants: An Update on the Immunopathology of Multisystem Inflammatory Syndrome in Children. 描述大象：儿童多系统炎症综合征免疫病理学的最新进展。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-06-07 DOI: 10.1080/08820139.2024.2363833

Sarah van den Berg, Thomas Sun

{"title":"Describing Elephants: An Update on the Immunopathology of Multisystem Inflammatory Syndrome in Children.","authors":"Sarah van den Berg, Thomas Sun","doi":"10.1080/08820139.2024.2363833","DOIUrl":"10.1080/08820139.2024.2363833","url":null,"abstract":"First described in 2020, multi-system inflammatory syndrome in children (MIS-C) is an, initially life-threatening, disease characterised by severe inflammation and following exposure to SARS-CoV-2. The immunopathology of MIS-C involves a hyperinflammation characterised by a cytokine storm and activation of both the innate and adaptive immune system, eventually leading to multi-organ failure. Several etiological theories are described in literature. Firstly, it is suggested that the gut plays an important role in the translocation of microbial products to the systemic circulation. Additionally, the production of autoantibodies that develop after the initial infection with SARS-CoV-2 might lead to many of its broad clinical symptoms. Finally, the superantigen theory where non-specific binding of the SARS-CoV-2 spike glycoprotein to the T-cell receptor leads to a subsequent activation of T cells, generating a powerful immune response. Despite the sudden outbreak of MIS-C and alarming messages, as of 2024, cases have declined drastically and subsequently show a less severe clinical spectrum. However, subacute cases not meeting current diagnostic criteria might be overlooked even though they represent a valuable research population. In the future, research should focus on adjusting these criteria to better understand the broad pathophysiology of MIS-C, aiding early detection, therapy, and prediction.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"962-974"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141283644","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

TMEM79 Ameliorates Cerebral Ischemia/Reperfusion Injury Through Regulating Inflammation and Oxidative Stress via the Nrf2/NLRP3 Pathway. TMEM79通过Nrf2/NLRP3途径调节炎症和氧化应激改善脑缺血再灌注损伤

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-05-29 DOI: 10.1080/08820139.2024.2354268

Wei Zhang, Chengcheng Fan, Zhongxue Yi, Tao Du, Nana Wang, Weizhu Tian, Qian Pan, Xiande Ma, Zhe Wang

{"title":"TMEM79 Ameliorates Cerebral Ischemia/Reperfusion Injury Through Regulating Inflammation and Oxidative Stress via the Nrf2/NLRP3 Pathway.","authors":"Wei Zhang, Chengcheng Fan, Zhongxue Yi, Tao Du, Nana Wang, Weizhu Tian, Qian Pan, Xiande Ma, Zhe Wang","doi":"10.1080/08820139.2024.2354268","DOIUrl":"10.1080/08820139.2024.2354268","url":null,"abstract":"Background: Cerebral ischemia/reperfusion injury (CIRI) is still a complicated disease with high fatality rates worldwide. Transmembrane Protein 79 (TMEM79) regulates inflammation and oxidative stress in some other diseases.Methods: CIRI mouse model was established using C57BL/6J mice through middle cerebral artery occlusion-reperfusion (MCAO/R), and BV2 cells were subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) to simulate CIRI. Brain tissue or BV2 cells were transfected or injected with lentivirus-carried TMEM79 overexpression vector. The impact of TMEM79 on CIRI-triggered oxidative stress was ascertained by dihydroethidium (DHE) staining and examination of oxidative stress indicators. Regulation of TMEM79 in neuronal apoptosis and inflammation was determined using TUNEL staining and ELISA.Results: TMEM79 overexpression mitigated neurological deficit induced by MCAO/R and decreased the extent of cerebral infarct. TMEM79 prevented neuronal death in brain tissue of MCAO/R mouse model and suppressed inflammatory response by reducing inflammatory cytokines levels. Moreover, TMEM79 significantly attenuated inflammation and oxidative stress caused by OGD/R in BV2 cells. TMEM79 facilitated the activation of Nrf2 and inhibited NLRP3 and caspase-1 expressions. Rescue experiments indicated that the Nrf2/NLRP3 signaling pathway mediated the mitigative effect of TMEM79 on CIRI in vivo and in vitro.Conclusion: Overall, TMEM79 was confirmed to attenuate CIRI via regulating the Nrf2/NLRP3 signaling pathway.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"872-890"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141160849","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

The Therapeutic Potential of Neutrophil Extracellular Traps and NLRP3 Inflammasomes in Mycoplasma pneumoniae Pneumonia. 中性粒细胞胞外陷阱和 NLRP3 炎症体在肺炎支原体肺炎中的治疗潜力

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-06-14 DOI: 10.1080/08820139.2024.2364796

Lei Yang, Cen Zhang, Yan Liu, Huijing Bao, Zhihua Wang

{"title":"The Therapeutic Potential of Neutrophil Extracellular Traps and NLRP3 Inflammasomes in Mycoplasma pneumoniae Pneumonia.","authors":"Lei Yang, Cen Zhang, Yan Liu, Huijing Bao, Zhihua Wang","doi":"10.1080/08820139.2024.2364796","DOIUrl":"10.1080/08820139.2024.2364796","url":null,"abstract":"Introduction: Mycoplasma pneumoniae (MP) is the most common pathogen of community-acquired pneumonia in children. However, the role of neutrophil extracellular traps (NETs) in the pathogenesis of MP is unclear.Methods: Both the level of NETs were detected between the 60 MP pneumonia patients and 20 healthy controls, whose the clinical characteristics were compared. Additionally, NETs formation induced by community-acquired respiratory distress syndrome (CARDS) toxin was also analyzed through transcriptome sequencing.Results: The levels of cell-free DNA, Cit-H3, and MPO-DNA complexes were significantly increased in the patients with MP pneumonia. Importantly, both cell-free DNA and LDH were higher in hospitalized patients with severity than those without severity. In addition, CARDS toxin induced the NETs formation in vitro and in vivo. Transcriptomics GO and KEGG pathway analysis indicate that NOD like receptor signaling pathway and Toll-like receptor signaling pathway are significantly enriched. Finally, we found that DNase I significantly attenuated the higher levels of Cit-H3, and up-regulation of interleukin-1β (IL-1β) and interleukin-18 (IL-18) by down-regulating the expression of NLRP3 and Caspase1(p20) in the lung tissues.Discussion: These results indicate that inhibiting excessive activation of NLRP3 inflammasomes, and NETs formation may alleviate MP pneumonia.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"975-988"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317059","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

Exploring the Significance of Microglial Phenotypes and Morphological Diversity in Neuroinflammation and Neurodegenerative Diseases: From Mechanisms to Potential Therapeutic Targets. 探索小胶质细胞表型和形态多样性在神经炎症和神经退行性疾病中的意义：从机制到潜在治疗靶点。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-06-05 DOI: 10.1080/08820139.2024.2358446

Mai M Anwar, Leonor Pérez-Martínez, Gustavo Pedraza-Alva

{"title":"Exploring the Significance of Microglial Phenotypes and Morphological Diversity in Neuroinflammation and Neurodegenerative Diseases: From Mechanisms to Potential Therapeutic Targets.","authors":"Mai M Anwar, Leonor Pérez-Martínez, Gustavo Pedraza-Alva","doi":"10.1080/08820139.2024.2358446","DOIUrl":"10.1080/08820139.2024.2358446","url":null,"abstract":"Studying various microglial phenotypes and their functions in neurodegenerative diseases is crucial due to the intricate nature of their phenomics and their vital immunological role. Microglia undergo substantial phenomic changes, encompassing morphological, transcriptional, and functional aspects, resulting in distinct cell types with diverse structures, functions, properties, and implications. The traditional classification of microglia as ramified, M1 (proinflammatory), or M2 (anti-inflammatory) phenotypes is overly simplistic, failing to capture the wide range of recently identified microglial phenotypes in various brain regions affected by neurodegenerative diseases. Altered and activated microglial phenotypes deviating from the typical ramified structure are significant features of many neurodegenerative conditions. Understanding the precise role of each microglial phenotype is intricate and sometimes contradictory. This review specifically focuses on elucidating recent modifications in microglial phenotypes within neurodegenerative diseases. Recognizing the heterogeneity of microglial phenotypes in diseased states can unveil novel therapeutic strategies for targeting microglia in neurodegenerative diseases. Moreover, the exploration of the use of healthy isolated microglia to mitigate disease progression has provided an innovative perspective. In conclusion, this review discusses the dynamic landscape of mysterious microglial phenotypes, emphasizing the need for a nuanced understanding to pave the way for innovative therapeutic strategies for neurodegenerative diseases.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"891-946"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247755","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

Serum YKL-40 and Serum Krebs von den Lungen-6 as Potential Predictive Biomarkers for Rheumatoid Arthritis-Associated Interstitial Lung Disease. 血清 YKL-40 和血清 Krebs von den Lungen-6 作为类风湿性关节炎相关间质性肺病的潜在预测性生物标记物。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-06-20 DOI: 10.1080/08820139.2024.2366966

Bo Liang, Yan Zhang, Dan Ke, Rui Yan, Min-Na Jiang, Li Li, Li-Xia Zhang, Xue-Gang Zhao, Guan-Ping Yuan, Bing Xu, Xiao-Min Liu

{"title":"Serum YKL-40 and Serum Krebs von den Lungen-6 as Potential Predictive Biomarkers for Rheumatoid Arthritis-Associated Interstitial Lung Disease.","authors":"Bo Liang, Yan Zhang, Dan Ke, Rui Yan, Min-Na Jiang, Li Li, Li-Xia Zhang, Xue-Gang Zhao, Guan-Ping Yuan, Bing Xu, Xiao-Min Liu","doi":"10.1080/08820139.2024.2366966","DOIUrl":"10.1080/08820139.2024.2366966","url":null,"abstract":"Background: Interstitial lung disease (ILD) is a common pulmonary manifestation of rheumatoid arthritis (RA) and is associated with a poor prognosis. However, the role of blood biomarkers in RA-associated interstitial lung disease (RA-ILD) is ill-defined. We aim to evaluate the role of YKL-40 and Krebs von den Lungen-6 (KL-6) in the diagnosis and severity evaluation of RA-ILD.Methods: 45 RA-non-ILD patients and 38 RA-ILD patients were included. The clinical data and the levels of YKL-40 and KL-6 were measured and collected for all patients. The risk factors for RA-ILD were analyzed and their correlation with relevant indicators and predictive value for RA-ILD was explored.Results: The levels of YKL-40 and KL-6 in RA-ILD patients were higher than RA-non-ILD patients (p < .001). Both YKL-40 and KL-6 were correlated with the incidence of RA-ILD. The predictive power of combined KL-6 and YKL-40 for the presence of ILD was 0.789, with a sensitivity and specificity at 73.7% and 73.3%, respectively. In RA-ILD patients, both YKL-40 and KL-6 were positively correlated with the Scleroderma Lung Study (SLS) I score and negatively correlated with pulmonary function.Conclusions: KL-6 and YKL-40 might be a useful biomarker in the diagnosis and severity evaluation of RA-ILD.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"989-1000"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141426801","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

Dysregulated MiR-223-5p Modulates Inflammation and Oxidative Stress in Traumatic Spinal Cord Injury. 失调的 MiR-223-5p 可调节创伤性脊髓损伤的炎症和氧化应激。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-05-30 DOI: 10.1080/08820139.2024.2359531

Dawei Wang, Yingshuang Wu, Yongxiang Liu, Qinghui Ji, Yi Luo, Jinglong Yan

{"title":"Dysregulated MiR-223-5p Modulates Inflammation and Oxidative Stress in Traumatic Spinal Cord Injury.","authors":"Dawei Wang, Yingshuang Wu, Yongxiang Liu, Qinghui Ji, Yi Luo, Jinglong Yan","doi":"10.1080/08820139.2024.2359531","DOIUrl":"10.1080/08820139.2024.2359531","url":null,"abstract":"Aim: This study aimed to evaluate the miR-223-5p expression in patients with spinal cord injury (SCI) and to determine its role in the pathogenesis of SCI.Methods: The serum miR-223-5p levels were analyzed using quantitative real-time polymerase chain reaction. The diagnostic accuracy of miR-223-5p was evaluated using the receiving operating characteristic curves. LPS-induced PC12 cells were established as an in vitro inflammatory cell model. Cell apoptosis, inflammation and oxidative stress were examined. The SCI rat model was constructed to evaluate the effects of miR-223-5p on inflammatory response and motor function in rats.Results: MiR-223-5p expression was upregulated in SCI patients. MiR-223-5p expression in the complete SCI group was significantly higher than that in incomplete SCI group. ROC analysis showed that miR-223-5p can distinguish SCI patients from healthy volunteers. In vitro experiments demonstrated that LPS upregulated apoptosis and inflammation in PC12 cells. Treatment with miR-223-5p inhibitor alleviated the changes in LPS-induced PC12 cells . Inhibition of miR-223-5p can alleviate the activation of inflammatory response and the effects of SCI on the motor function in rats.Conclusions: MiR-223-5p is a potential diagnostic marker for SCI, and it can promote the SCI progression by regulating nerve cell survival, inflammation, and oxidative stress.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"947-961"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141175428","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

Efficacy of IFN-γ, sCD40L, and Poly(I:C) Treated Bone Marrow-Derived Macrophages in Murine Mammary Carcinoma. 经 IFN-γ、sCD40L 和 Poly(I:C) 处理的骨髓衍生巨噬细胞对鼠乳腺癌的疗效

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-05-30 DOI: 10.1080/08820139.2024.2354264

Meghan Roberts, Joshua Finn, Melissa Lass, Ernesto Oviedo-Bermudez, Robert A Kurt

{"title":"Efficacy of IFN-γ, sCD40L, and Poly(I:C) Treated Bone Marrow-Derived Macrophages in Murine Mammary Carcinoma.","authors":"Meghan Roberts, Joshua Finn, Melissa Lass, Ernesto Oviedo-Bermudez, Robert A Kurt","doi":"10.1080/08820139.2024.2354264","DOIUrl":"10.1080/08820139.2024.2354264","url":null,"abstract":"Introduction: Here, we explored methods to generate anti-tumor bone marrow-derived macrophages (BMDM) and how delivery of the BMDM at early tumor sites could impact disease progression.Methods: BMDM treated with IFN-γ, sCD40L, poly(I:C), and a combination of the three were assessed.Results: Treatment with sCD40L had no significant impact on the BMDM. Treating BMDM with IFN-γ impacted IL-1β, MHC Class II, and CD80 expression. While poly(I:C) treatment had a greater impact on the BMDM than IFN-γ when assessed by the in vitro assays, the BMDM treated with poly (I:C) had mixed results in vivo where they decreased growth of the EMT6 tumor, did not impact growth of the 168 tumor, and enhanced growth of the 4T1 tumor. The combination of poly(I:C), IFN-γ, and sCD40L had the greatest impact on the BMDM in vitro and in vivo. Treatment with all three agonists resulted in increased IL-1β, TNF-α, and IL-12 expression, decreased expression of arginase and mrc, increased phagocytic activity, nitrite production, and MHC Class II and CD80 expression, and significantly impacted growth of the EMT6 and 168 murine mammary carcinoma models.Discussion: Collectively, these data show that treating BMDM with poly(I:C), IFN-γ, and sCD40L generates BMDM with more consistent anti-tumor activity than BMDM generated with the individual agonists.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"857-871"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141175435","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

Differential GPR56 Expression in T Cell Subpopulations for Early-Stage Lung Adenocarcinoma Patient Identification. 用于早期肺腺癌患者识别的 T 细胞亚群中 GPR56 的差异表达。

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-08-01 Epub Date: 2024-05-29 DOI: 10.1080/08820139.2024.2350549

Jiaxin Ren, Yaoyi Zhu, Yuying Nie, Mohan Zheng, Ainizati Hasimu, Ming Zhao, Yiming Zhao, Xiancan Ma, Zihang Yuan, Qi Li, Ayibaota Bahabayi, Zhonghui Zhang, Xingyue Zeng, Chen Liu

{"title":"Differential GPR56 Expression in T Cell Subpopulations for Early-Stage Lung Adenocarcinoma Patient Identification.","authors":"Jiaxin Ren, Yaoyi Zhu, Yuying Nie, Mohan Zheng, Ainizati Hasimu, Ming Zhao, Yiming Zhao, Xiancan Ma, Zihang Yuan, Qi Li, Ayibaota Bahabayi, Zhonghui Zhang, Xingyue Zeng, Chen Liu","doi":"10.1080/08820139.2024.2350549","DOIUrl":"10.1080/08820139.2024.2350549","url":null,"abstract":"Objective: This study aimed to investigate the expression of GPR56 in the T cells of early-stage lung adenocarcinoma (LUAD) patients and clarify its diagnostic significance.Methods: Blood samples were collected from 32 patients with stage IA LUAD and 31 healthy controls. GPR56 and perforin were analysed in circulating T-cell subsets by flow cytometry. In addition, a correlation between perforin and GPR56 expression was detected. Changes in GPR56+ cells in early LUAD patients were analysed, and the diagnostic significance of GPR56+ T cells for early LUAD was studied by receiver operating characteristic (ROC) curve analysis.Results: The expression of GPR56 in CD8+ T cells from early-stage LUAD patients was significantly greater than that in CD4+ T cells. The percentage of perforin-positive GPR56+ cells in early-stage LUAD patients was high. GPR56 levels in the T cells of LUAD patients were significantly lower than those in healthy controls. ROC analysis revealed that the area under the curve for the percentage of GPR56-positive CD8+ TEMRA cells to distinguish early-stage LUAD patients from healthy individuals- reached 0.7978.Conclusion: The decreased expression of GPR56 in the peripheral blood of early-stage LUAD patients correlated with perforin levels, reflecting compromised antitumor immunity and aiding early-stage LUAD screening.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"843-856"},"PeriodicalIF":2.9,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141160842","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

Impact of siRNA-Mediated Cofilin-1 Knockdown and Obesity Associated Microenvironment on the Motility of Natural Killer Cells. siRNA 引导的 Cofilin-1 敲除和肥胖相关微环境对自然杀伤细胞运动性的影响

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-07-01 Epub Date: 2024-05-09 DOI: 10.1080/08820139.2024.2327327

Bruno Griesler, Marijke Hölzel, Jana Oswald, Johannes Fänder, Trutz Fischer, Maximilian Büttner, Dagmar Quandt, Ina Bähr, Simon Jasinski-Bergner, Ivonne Bazwinsky-Wutschke, Heike Kielstein

{"title":"Impact of siRNA-Mediated Cofilin-1 Knockdown and Obesity Associated Microenvironment on the Motility of Natural Killer Cells.","authors":"Bruno Griesler, Marijke Hölzel, Jana Oswald, Johannes Fänder, Trutz Fischer, Maximilian Büttner, Dagmar Quandt, Ina Bähr, Simon Jasinski-Bergner, Ivonne Bazwinsky-Wutschke, Heike Kielstein","doi":"10.1080/08820139.2024.2327327","DOIUrl":"10.1080/08820139.2024.2327327","url":null,"abstract":"The anti-tumor capacity of natural killer (NK) cells heavily relies on their ability to migrate towards their target cells. This process is based on dynamic actinrearrangement, so-called actin treadmilling, andis tightly regulated by proteins such as cofilin-1. The aim of the present study was to identify the role of cofilin-1 (CFL-1) in the migratory behavior of NK cells and to investigate a possible impact of an obesity-associated micromilieu on these cells, as it is known that obesity correlates with various impaired NK cell functions. CFL-1 was knocked-down via transfection of NK-92 cells with respective siRNAs. Obesity associated micromilieu was mimicked by incubation of NK-92 cells with adipocyte-conditioned medium from human preadipocyte SGBS cells or leptin. Effects on CFL-1 levels, the degree of phosphorylation to the inactive pCFL-1 as well as NK-92 cell motility were analyzed. Surprisingly, siRNA-mediated CFL-1 knockdown led to a significant increase of migration, as determined by enhanced velocity and accumulated distance of migration. No effect on CFL-1 nor pCFL-1 expression levels, proportion of phosphorylation and cell migratory behavior could be demonstrated under the influence of an obesity-associated microenvironment. In conclusion, the results indicate a significant effect of a CFL-1 knockdown on NK cell motility.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"713-729"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896076","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

Genetic Association of Interleukin 16 Gene Polymorphisms (rs11556218 & rs4778889) with Type 1 Diabetes in Egyptian Children: A Case-Control Study. 埃及儿童白细胞介素 16 基因多态性（rs11556218 和 rs4778889）与 1 型糖尿病的遗传关系：病例对照研究

IF 2.9 4区医学

Immunological Investigations Pub Date : 2024-07-01 Epub Date: 2024-05-21 DOI: 10.1080/08820139.2024.2349034

Yasser B M Ali, Mai M Saed, Nehal E Abdel-Hakem, Mona Abd Elmotaleb A Hussein, Mohamed El-Shahat

{"title":"Genetic Association of Interleukin 16 Gene Polymorphisms (rs11556218 & rs4778889) with Type 1 Diabetes in Egyptian Children: A Case-Control Study.","authors":"Yasser B M Ali, Mai M Saed, Nehal E Abdel-Hakem, Mona Abd Elmotaleb A Hussein, Mohamed El-Shahat","doi":"10.1080/08820139.2024.2349034","DOIUrl":"10.1080/08820139.2024.2349034","url":null,"abstract":"Background: Type 1 diabetes (T1D) is a serious chronic autoimmune condition. Even though the underlying reason for the onset of T1D is unknown, due to their effector and regulatory roles in immune responses, cytokines are essential in developing autoimmune disorders. Interleukin (IL)16 is an immunomodulatory cytokine implicated in several inflammatory and autoimmune diseases.Objective: This study was designed to examine the association of IL16 gene polymorphisms, rs11556218 T > G and rs4778889 T > C, with the risk of T1D in Egyptian children.Methods: Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay, we analyzed rs11556218 T > G and rs4778889 T > C polymorphisms of the IL16 gene in 100 T1D subjects and 93 controls.Results: Rs11556218 T > G polymorphism of the IL16 gene was not associated with the risk of developing T1D. Analysis of IL16 gene rs4778889 T > C showed that the TT genotype had a considerably higher risk of T1D than the TC genotype [OR = 2.195 (1.205-3.999)]. In comparison to patients with the C allele [OR = 0.6914 (0.38-1.2569)], patients with the T allele [OR = 1.45 (0.7956-2.6296)] were notably more likely to have T1D. A significant decrease was found in the frequency of GT (OR = 0.43, p = .03) and TC (OR = 0.32, p = .011) haplotypes of IL16 gene rs11556218 T > G and rs4778889 T > C polymorphisms in T1D patients compared with controls.Conclusion: IL16 gene rs4778889 T > C polymorphism might be associated with susceptibility to T1D. Egyptians with TT genotypes are more likely to develop T1D. However, GT and TC haplotypes of IL16 gene rs11556218 T > G and rs4778889 T > C polymorphisms highlight their protective role againstT1D disease.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"830-842"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075926","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