Journal of cellular immunology最新文献_第3页

Sharing Weal and Woe: A Commentary on “Gasdermin E Regulates the Stability and Activation of EGFR in Human Non-Small Cell Lung Cancer Cells” 同甘共苦:《气皮蛋白E调控人非小细胞肺癌细胞EGFR的稳定性和活化》述评

Journal of cellular immunology Pub Date : 2023-07-17 DOI: 10.33696/immunology.5.167

Limei Xu, Xiangguo Liu

{"title":"Sharing Weal and Woe: A Commentary on “Gasdermin E Regulates the Stability and Activation of EGFR in Human Non-Small Cell Lung Cancer Cells”","authors":"Limei Xu, Xiangguo Liu","doi":"10.33696/immunology.5.167","DOIUrl":"https://doi.org/10.33696/immunology.5.167","url":null,"abstract":"Abnormal activation of epidermal growth factor receptor (EGFR) promotes the development of Non-Small Cell Lung Cancer Cells (NSCLC). Chemoresistance to tyrosine kinase inhibitors (TKIs), which is elicited by EGFR mutations, is a key challenge for NSCLC treatment. In the present study, we demonstrate a critical role of gasdermin E (GSDME), an important protein for pyroptosis, in the maintenance of EGFR stability and activation. We found that GSDME depletion suppressed the EGFR-mediated proliferation of NSCLC cells in vitro. GSDME knockdown downregulated the protein level of CCND1 and inhibited the phosphorylation of ERK1/2 in NSCLC cells. Mechanistically, both GSDME-FL and GSDME-N fragment physically interacted with EGFR. GSDME interacted with cytoplasmic fragment (CT) of EGFR. GSDME knockdown inhibited EGFR dimerization and phosphorylation at tyrosine 1173 (EGFRY1173), which could activate ERK1/2. GSDME knockdown promoted EGFR degradation and phosphorylation at tyrosine 1045 (EGFRY1045). Importantly, GSDME-FL increased the stability of EGFR, while the GSDME-N fragment induced EGFR degradation. Together, our results demonstrate that the GSDME-EGFR interaction plays an important role in NSCLC development, reveal a previously unrecognized link between GSDME and EGFR stability and offer new insight into cancer pathogenesis.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44144853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 Potential of Probiotics in Boosting the Immune System's Response to Reduce the Severity of Malaria 探索益生菌在增强免疫系统反应以降低疟疾严重程度方面的潜力

Journal of cellular immunology Pub Date : 2023-05-24 DOI: 10.33696/immunology.5.166

Bamgbose Timothy, J. de la Fuente

引用次数: 1

Is Interstitial Macrophage Mainly Responsible for Lung Injury in SARS-CoV-2 Infection? 间质巨噬细胞是严重急性呼吸系统综合征冠状病毒2型感染肺损伤的主要原因吗？

Journal of cellular immunology Pub Date : 2023-04-29 DOI: 10.33696/immunology.5.165

José Guillermo Cabanillas López

引用次数: 0

Role of Granulocyte-Colony Stimulating Factor (G-CSF) in Immune Regulation and Neuroprotection 粒细胞集落刺激因子(G-CSF)在免疫调节和神经保护中的作用

Journal of cellular immunology Pub Date : 2023-03-23 DOI: 10.33696/immunology.5.156

引用次数: 0

Intracellular Hyaluronan Synthesis Impairs Hematopoiesis in Diabetes that can be Prevented by Heparin 细胞内透明质酸合成损害糖尿病患者造血功能，可通过肝素预防

Journal of cellular immunology Pub Date : 2023-03-23 DOI: 10.33696/immunology.5.155

A. Wang, V. Hascall

引用次数: 0

From Lipase Elevation to Diabetes – Pancreatic Involvement during Immune Checkpoint Inhibition 从脂肪酶升高到糖尿病——免疫检查点抑制过程中胰腺的参与

Journal of cellular immunology Pub Date : 2023-03-23 DOI: 10.33696/immunology.5.158

引用次数: 1

Importance of Ultrasensitive ELISA in Cancer Research 超敏ELISA在癌症研究中的重要意义

Journal of cellular immunology Pub Date : 2023-03-23 DOI: 10.33696/immunology.5.157

引用次数: 0

Towards a Chemo-immunotherapy to Improve Breast Cancer Immunotherapy 化学免疫疗法改善乳腺癌免疫治疗

Journal of cellular immunology Pub Date : 2023-03-23 DOI: 10.33696/immunology.5.159

引用次数: 0

The High Fat Diet Impacts the Plasticity between Fresh and Aged Neutrophils. 高脂饮食影响新鲜和老化中性粒细胞之间的可塑性

Journal of cellular immunology Pub Date : 2023-01-01 DOI: 10.33696/immunology.5.182

Andrea Baragetti, Giuseppe Danilo Norata

{"title":"The High Fat Diet Impacts the Plasticity between Fresh and Aged Neutrophils.","authors":"Andrea Baragetti, Giuseppe Danilo Norata","doi":"10.33696/immunology.5.182","DOIUrl":"10.33696/immunology.5.182","url":null,"abstract":"Metabolic alterations induced by unhealthy lifestyles, including obesity and insulin resistance are often associated with increased innate immune response and chronic inflammation. Cholesterol has been identified as a key metabolite driving the activation of the inflammasome and the \"epigenetic memory\" in long-term living hematopoietic stem cells. In addition to these mechanisms, the physiological aging of short-living neutrophils is a relevant modifier of their immune competency, as while they egress from medullary niches as \"fresh\", fully competent, cells, they turn into \"aged\", disarmed cells, when they extravasate into peripheral tissues to fight against pathogens or they reach the spleen for disposal. We recently observed that cardio-metabolic alterations induced by a lipid enriched unhealthy diet critically accelerate this process. Indeed, the chronic feeding with a high fat diet (HFD) results in the increase of aged neutrophils in the circulation and their accumulation in liver. This profile is associated with a deteriorated insulin response and obesity. The HFD primes aged, but not fresh neutrophils, to infiltrate in the liver and promotes inflammation coupled to altered cell immune architecture in visceral adipose tissue. Preventing the aging of neutrophils via selective ablation of CXCR2, reduces the development of obesity and improves the sensitivity to insulin. In humans, plasma levels of CXCL1, one of the cytokines binding CXCR2 and promoting neutrophil aging, are directly associated with abdominal adiposity and fatty liver independently of other risk factors. Together these findings point to a direct role of aged neutrophils in the development of metabolic disorders.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"5 5","pages":"168-173"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7615605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139704195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunologic Implications for Stroke Recovery: Unveiling the Role of the Immune System in Pathogenesis, Neurorepair, and Rehabilitation. 中风康复的免疫学意义：揭示免疫系统在发病机制、神经修复和康复中的作用。

Journal of cellular immunology Pub Date : 2023-01-01 DOI: 10.33696/immunology.5.170

Grace Hey, Siya Bhutani, Maxwell Woolridge, Aashay Patel, Anna Walls, Brandon Lucke-Wold

{"title":"Immunologic Implications for Stroke Recovery: Unveiling the Role of the Immune System in Pathogenesis, Neurorepair, and Rehabilitation.","authors":"Grace Hey, Siya Bhutani, Maxwell Woolridge, Aashay Patel, Anna Walls, Brandon Lucke-Wold","doi":"10.33696/immunology.5.170","DOIUrl":"10.33696/immunology.5.170","url":null,"abstract":"Stroke is a debilitating neurologic condition characterized by an interruption or complete blockage of blood flow to certain areas of the brain. While the primary injury occurs at the time of the initial ischemic event or hemorrhage, secondary injury mechanisms contribute to neuroinflammation, disruption of the blood-brain barrier (BBB), excitotoxicity, and cerebral edema in the days and hours after stroke. Of these secondary mechanisms of injury, significant dysregulation of various immune populations within the body plays a crucial role in exacerbating brain damage after stroke. Pathological activity of glial cells, infiltrating leukocytes, and the adaptive immune system promote neuroinflammation, BBB damage, and neuronal death. Chronic immune activation can additionally encourage the development of neurologic deficits, immunosuppression, and dysregulation of the gut microbiome. As such, immunotherapy has emerged as a promising strategy for the clinical management of stroke in a highly patient-specific manner. These strategies include regulatory T cells (Tregs), cell adhesion molecules, cytokines, and monoclonal antibodies. However, the use of immunotherapy for stroke remains largely in the early stages, highlighting the need for continued research efforts before widespread clinical use.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"5 3","pages":"65-81"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49685821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0