Journal of cellular immunology最新文献

{"title":"FLIP-expressing myeloid cells as driver of systemic immune disorders","authors":"Alberto Atanasio, D. Rizzini, S. Ugel","doi":"10.33696/immunology.4.138","DOIUrl":"https://doi.org/10.33696/immunology.4.138","url":null,"abstract":"The role of FLIP as a moonlighting protein is becoming progressively evident since this protein is often involved in various processes correlated to aberrant immunological responses independently from its function as master anti-apoptotic regulator. It has been uncovered that FLIP drives the acquisition of immunosuppression and inflammation-associated pathways in myeloid cells. The clinical picture raised during SARS-CoV-2 pandemic has given the possibility to deeply investigate FLIP involvement in releasing a systemic cytokine storm, also linked to a chronic inflammatory syndrome associated with immune suppression and cancer progression. Indeed, a FLIP/STAT3 axis orchestrates an aberrant inflammatory program in myeloid cells of COVID-19 patients and SARS-CoV-2 infected hACE2 transgenic mice. Moreover, the same activated FLIP/STAT3 axis was confirmed in a chimeric vFLIP mouse model, where vFLIP overexpression was restricted exclusively in myeloid cells by using a tissue-specific CRE-driver (e.g., LysMCre mice), validating this model as a feasible platform to study the late phase of COVID-19 disease. The STAT3 pro-inflammatory pathway triggered by the aberrant expression of FLIP in myeloid cells well correlates to the outcome of the cytokine release syndrome (CRS) that is the latest and most severe phase in COVID-19 disease confirming FLIP-mediated myeloid reprogramming as a cornerstone of systemic immune disorders.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45561195","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}

{"title":"LncZFAS1 Inhibit MPP+-Induced Neuroinflammation Through TXNIP/MIB1 E3 Ubiquitin Ligase/NLRP3 Axis","authors":"","doi":"10.33696/immunology.4.134","DOIUrl":"https://doi.org/10.33696/immunology.4.134","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47610971","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}

{"title":"Sticky Interactions in Lupus Nephritis","authors":"","doi":"10.33696/immunology.4.126","DOIUrl":"https://doi.org/10.33696/immunology.4.126","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45320621","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}

{"title":"Towards a Better Understanding of Staphylococcus aureus Skin Infections-The Interactions with Dendritic Cells","authors":"","doi":"10.33696/immunology.4.127","DOIUrl":"https://doi.org/10.33696/immunology.4.127","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42779107","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}

{"title":"Glucose Metabolism is a Better Marker for Predicting Clinical Alzheimer’s Disease than Amyloid or Tau","authors":"Tyler C. Hammond, Ai-Ling Lin","doi":"10.33696/immunology.4.128","DOIUrl":"https://doi.org/10.33696/immunology.4.128","url":null,"abstract":"Alzheimer’s disease (AD) research has long been dominated with communications regarding the amyloid hypothesis and targeting amyloid clearance through pharmacological therapies from the brain [1]. Unfortunately, this research strategy has yielded only one new FDA-accelerated approved therapeutic for early AD, and its clinical benefit still needs to be verified [2]. It may be time to employ a new strategy in AD therapeutics research. Hammond et al. reported that diminished uptake of glucose in the brain is a better marker for classifying AD than beta-amyloid (A β ) or phosphorylated tau deposition [3]. The National Institute on Aging and the Alzheimer’s Association published revised guidelines for the diagnosis of AD to include the measurement of amyloid (A), tau (T), and neurodegeneration (N), when diagnosing and treating AD [4]. It is highly relevant to AD therapeutic research whether amyloid, tau, and neurodegeneration contribute equally to the progression of AD at all phases of the disease or in a matter dependent on disease phase. To be able to successfully treat or prevent AD, there is a pressing need to identify precision biomarkers that are sensitive to disease progression and able to predict onset of cognitive impairment [5]. Hammond et al. used an advanced statistical learning machine learning method, random forest, on data provided by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) to measure the ability of beta-amyloid measured by positron emission tomography (A β -PET), phosphorylated tau measured in the cerebral spinal fluid (CSF-pTau), fluorodeoxyglucose measured by positron emission tomography (FDG-PET) and structural imaging measured by magnetic resonance imaging (MRI) to classify AD diagnosis. Their results demonstrated that amyloid, tau, and neurodegeneration have a phase-dependent impact on the development of AD. A β and pTau are better predictors of the early dementia status that is often defined as mild cognitive impairment (MCI), and neurodegeneration, especially low glucose uptake, is a better predictor of later dementia status, or clinical AD. A","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"4 1","pages":"15 - 18"},"PeriodicalIF":0.0,"publicationDate":"2022-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42196487","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}

{"title":"Glucose Metabolism is a Better Marker for Predicting Clinical Alzheimer's Disease than Amyloid or Tau.","authors":"Tyler C Hammond, Ai-Ling Lin","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"4 1","pages":"15-18"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8975178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9704016","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}

{"title":"PD-L1 as a Novel Mediator of Lung Fibroblast to Myofibroblast Transition.","authors":"Xia Guo, Guoqing Qian","doi":"10.33696/immunology.4.142","DOIUrl":"https://doi.org/10.33696/immunology.4.142","url":null,"abstract":"of levels of high PD-L1","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"4 4","pages":"141-144"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40512816","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}

{"title":"Comparison of Gene Editing versus a Neutrophil Elastase Inhibitor as Potential Therapies for <i>ELANE</i> Neutropenia.","authors":"Vahagn Makaryan,&nbsp;Merideth Kelley,&nbsp;Breanna Fletcher,&nbsp;Isabella Archibald,&nbsp;Tanoya Poulsen,&nbsp;David Dale","doi":"10.33696/immunology.4.129","DOIUrl":"https://doi.org/10.33696/immunology.4.129","url":null,"abstract":"<p><p>Heterozygous mutations in <i>ELANE</i>, the gene for neutrophil elastase, cause cyclic and congenital neutropenia through the programed cell death of neutrophil progenitors in the bone marrow. Granulocyte colony-stimulating factor is an effective therapy for these diseases, but alternative therapies are needed, especially for patients who do not respond well or are at high risk of developing myeloid malignancies. We developed an HL60 cell model for <i>ELANE</i> neutropenia and previously demonstrated that transient and regulated expression of mutant <i>ELANE</i> causes cell death by accelerated apoptosis. Knocking down the mutant gene or exposure to a potent inhibitor of neutrophil elastase rescued neutrophil development. Because of the great diversity in causative <i>ELANE</i> mutations, we generated stable HL60 clones expressing mutant P139L, C151Y and G214R and compared the effects of elastase inhibitor exposure to an <i>ELANE</i> knock-out line on cell development and function. ATRA induced differentiation demonstrated comparably impaired myeloid cell development for all three lines with upregulated expression of GRP78/BIP, an abnormality corrected by exposure of these cells to the elastase inhibitor MK-0339. The inhibitor and KO of mutant <i>ELANE</i> led to formation of neutrophils with comparable chemotactic and bactericidal capacities. We concluded that both strategies have great potential for the treatment of cyclic and congenital neutropenia. However, an orally absorbed, cell permeable inhibitor of neutrophil elastase, if proven safe and effective in a clinical trial, might be the better alternative to G-CSF or gene editing to treat <i>ELANE</i> neutropenia.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":"19-28"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9431957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40342901","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}

{"title":"Commentary: Experimental Mouse Models of Invasive Candidiasis Caused by <i>Candida auris</i> and Other Medically Important <i>Candida</i> Species.","authors":"Hong Xin","doi":"10.33696/immunology.4.130","DOIUrl":"https://doi.org/10.33696/immunology.4.130","url":null,"abstract":"<p><p>The study \"<b>\"Experimental Mouse Models of Disseminated <i>Candida auris</i> Infection\"</b> provides the first insight into the critical role of C5 in the host antimicrobial defense to <i>disseminated candidiasis caused by C. auris</i>. This study also establishes an inbred A/J mouse model of systemic <i>C. auris</i> infection without drug-induced immunosuppression. <i>C. auris</i> has become the first fungal pathogen causing global public health threat due to its multidrug resistance (MDR) and persistence in hospital and nursing home settings. Currently, as compared to <i>C. albicans</i>, very limited animal models are available to study the progression of non<i>-albicans Candida</i> (NAC) species including <i>C. auris</i>. We have successfully established immunosuppressed C57BL/6, BALB/c and A/J murine models of disseminated candidiasis caused by five clinically significant <i>Candida</i> species: <i>C</i>. <i>albicans, C. glabrata, C. tropicalis, C. parapsilosis</i> and <i>C. auris</i>. Here we also report updated progress of some important mouse models for <i>C. auris</i> infection in the field. These valuable mouse models can be used for the assessment of antifungal drugs, evaluation of potential vaccines and monoclonal antibodies (mAbs) to protect before and after candidiasis, and comparison of pathogenicity of different <i>Candida</i> species.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":"29-33"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9286494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40624911","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}

{"title":"The Issue of Monocyte Activation in ASD: Troubles with Translation.","authors":"R J Moreno,&nbsp;P Ashwood","doi":"10.33696/immunology.4.146","DOIUrl":"https://doi.org/10.33696/immunology.4.146","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) prevalence has increased year on year for the past two decades and currently affects 1 in 44 individuals in the US. An increasing number of studies have pointed to increased immune activation as both an etiological agent and also involved in the ongoing pathological process of ASD. Both adaptive and innate immune responses have been implicated. Evidence of innate dysregulation has so far included increased production of innate inflammatory cytokines, increased cell numbers, and altered activation in monocytes in the blood and microglia in the brain. Suggesting an orchestrated innate immune response may be involved in ASD. Hughes et al. (2022) recently assessed transcriptome differences that could underlie altered activation of monocytes using next-generation bulk-RNA sequencing on isolated CD14+ monocytes at baseline and after activation with different Toll-like receptor agonists. Circulating CD14+ monocyte from children with autistic disorder (AD) and children diagnosed with perverse developmental disorder not otherwise specified (PDD-NOS) were found to differ in a number of activation pathways after gene enrichment analysis compared to typically developing children. There was an overall upregulation in translational machinery in both neurodevelopmental disorder groups, whereas typically developing children were downregulated, indicating an issue with monocyte activation. Several identified differentially expressed genes in monocytes were also identified as ASD at-risk genes, according to the Simons Foundation Autism Research Initiative (SFARI), and genes involved in inflammatory bowel diseases. This work implicates altered monocyte activation with a lack of regulation as a potential mechanistic issue in ASD. Future work is warranted to evaluate how monocyte regulatory mechanisms differ in ASD individuals.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"4 5","pages":"167-170"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9853954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10618696","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}