Journal of Immunology Research最新文献_第10页

Risk Prediction Models for Invasive Mechanical Ventilation in Patients with Autoimmune Encephalitis: A Retrospective Cohort Study 自身免疫性脑炎患者有创机械通气的风险预测模型:一项回顾性队列研究

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-12-05 DOI: 10.1155/2023/6616822

Shiyang Xie, Meilin Chen, Luying Qiu, Long Li, Shumin Deng, Fang Liu, Hefei Fu, Yanzhe Wang

{"title":"Risk Prediction Models for Invasive Mechanical Ventilation in Patients with Autoimmune Encephalitis: A Retrospective Cohort Study","authors":"Shiyang Xie, Meilin Chen, Luying Qiu, Long Li, Shumin Deng, Fang Liu, Hefei Fu, Yanzhe Wang","doi":"10.1155/2023/6616822","DOIUrl":"https://doi.org/10.1155/2023/6616822","url":null,"abstract":"Background and Objectives. Timely identification of developing severe respiratory failure in patients with autoimmune encephalitis (AE) is crucial to ensure prompt treatment with invasive mechanical ventilation (IMV), which can potentially improve the outcome. We aimed to develop a nomogram for requiring IMV based on easily available clinical characteristics. Methods. A multivariate predictive nomogram model was developed using the risk factors identified by LASSO regression and assessed by receiver operator characteristics (ROC) curve, calibration curve, and decision curve analysis. Results. The risk factors predictive of severe respiratory failure were male gender, impaired hepatic function, elevated intracranial pressure, and higher neuron-specific enolase. The final nomogram achieved an AUC of 0.770. After validation by bootstrapping, a concordance index of 0.748 was achieved. Conclusions. Our nomogram accurately predicted the risk of developing respiratory failure needing IMV in AE patients and provide clinicians with a simple and effective tool to guide treatment interventions in the AE patients.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":" 7","pages":""},"PeriodicalIF":4.1,"publicationDate":"2023-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138492850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Identification and Development of Synovial B-Cell-Related Genes Diagnostic Signature for Rheumatoid Arthritis. 类风湿关节炎滑膜b细胞相关基因诊断标志的鉴定和发展。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-11-25 eCollection Date: 2023-01-01 DOI: 10.1155/2023/9422990

Jifeng Tang, Jinfang Xia, Huiming Sheng, Jinpiao Lin

{"title":"Identification and Development of Synovial B-Cell-Related Genes Diagnostic Signature for Rheumatoid Arthritis.","authors":"Jifeng Tang, Jinfang Xia, Huiming Sheng, Jinpiao Lin","doi":"10.1155/2023/9422990","DOIUrl":"10.1155/2023/9422990","url":null,"abstract":"Background: The aim of the study was to investigate the landscape of B-cell-related gene expression profiling in rheumatoid arthritis (RA) synovium and explore the biological and clinical significance of these genes in RA.Methods: Expression profiling of synovial biopsies from subjects with 152 RA patients, 22 osteoarthritis (OA) patients, and 28 healthy controls was downloaded from the Gene Expression Omnibus database. Single-sample gene set enrichment analysis (ssGSEA) was performed to evaluate the abundance of infiltrated immune cells, and the results were validated using immunohistochemical staining. GSEA was employed to decipher differences in B-cell-related biological pathways. B-cell-related differential expression genes (BRDEGs) were screened, and BRDEGs-based model was developed by machine learning algorithms and evaluated by an external validation set and clinical RA cohort, then biological functions were further analyzed.Results: High levels of immune cell infiltration and B-cell-related pathway activation were revealed in RA synovium. BRDEGs were screened, and three key molecular markers consisting of FAS, GPR183, and TFRC were identified. The diagnosis model was established, and these gene markers have good discriminative ability for RA. Molecular pathological evaluation confirmed RA patients with high-risk scores presented higher levels of B-cell activation and RA characteristics. In addition, a competitive endogenous RNA network was established to elucidate the molecular mechanisms of the posttranscriptional network.Conclusions: We described the B-cell-related molecular landscape of RA synovium and constructed a molecular diagnostic model in RA. The three genes FAS, GPR183, and TFRC may be potential targets for clinical diagnosis and immunoregulatory therapy of RA.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"9422990"},"PeriodicalIF":4.1,"publicationDate":"2023-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10693468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138477869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EGF-Receptor against Amphiregulin (AREG) Influences Costimulatory Molecules on Monocytes and T Cells and Modulates T-Cell Responses. 抗双调节蛋白egf受体(AREG)影响单核细胞和T细胞的共刺激分子并调节T细胞反应。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-11-24 eCollection Date: 2023-01-01 DOI: 10.1155/2023/8883045

Stephan Dreschers, Christopher Platen, Louise Oppermann, Caitlin Doughty, Andreas Ludwig, Aaron Babendreyer, Thorsten W Orlikowsky

{"title":"EGF-Receptor against Amphiregulin (AREG) Influences Costimulatory Molecules on Monocytes and T Cells and Modulates T-Cell Responses.","authors":"Stephan Dreschers, Christopher Platen, Louise Oppermann, Caitlin Doughty, Andreas Ludwig, Aaron Babendreyer, Thorsten W Orlikowsky","doi":"10.1155/2023/8883045","DOIUrl":"10.1155/2023/8883045","url":null,"abstract":"Amphiregulin (AREG) is a ligand of the epidermal growth factor receptor (EGFR) and has been shown to regulate the phagocytosis-induced cell death of monocytes in peripheral blood. AREG-dependent apoptotic signaling engages factors of the intrinsic and extrinsic apoptotic pathway, such as BCL-2, BCL-XL, and death ligand/receptor CD95/CD95L. Here, we tested the hypothesis that AREG influences costimulatory monocyte functions, which are crucial for T-cell responses. We found a stronger expression of AREG and EGFR in monocytes compared to lymphocytes. As a novel function of AREG, we observed reduced T-cell proliferation following polyclonal T-cell stimulation with OKT3. This reduction of proliferation occurred in the presence of monocytes as well as in their absence, monocyte signaling being replaced by crosslinking of OKT3. Increasing concentrations of AREG down-modulated the concentration of costimulatory B7 molecules (CD80/CD86) and HLA-DR on monocytes. In proliferation assays, CD28 expression on T cells was down-modulated on the application of OKT3 but unaltered by AREG. LcK activation, following OKT3-stimulation, was reduced in T cells that had been coincubated with AREG. The effects of AREG on T-cell phenotypes were also present when monocytes were depleted and OKT3 was crosslinked. The rearranged expression of immunological synapse proteins was accompanied by an alteration of T-cell polarization. Although the proportion of regulatory T cells was not shifted by AREG, IL-17-expressing T cells were significantly enhanced, with a bias toward TH1-polarization. Taken together, these results suggest that AREG acts as an immunoregulatory molecule at the interface between antigen-presenting cells and T cells.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"8883045"},"PeriodicalIF":4.1,"publicationDate":"2023-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10691888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138477868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting Neutrophil Extracellular Traps: A Novel Antitumor Strategy 靶向中性粒细胞胞外陷阱:一种新的抗肿瘤策略

3区医学

Journal of Immunology Research Pub Date : 2023-11-09 DOI: 10.1155/2023/5599660

Hao Zuo, Mengjie Yang, Qian Ji, Shengqiao Fu, Xi Pu, Xu Zhang, Xu Wang

引用次数: 0

Sestrin2 Regulates Endoplasmic Reticulum Stress-Dependent Ferroptosis to Engage Pulmonary Fibrosis by Nuclear Factor Erythroid 2-Related Factor 2/Activating Transcription Factor 4 (NRF2/ATF4) Sestrin2通过核因子红系2相关因子2/激活转录因子4 (NRF2/ATF4)调控内质网应激依赖性铁凋亡参与肺纤维化

3区医学

Journal of Immunology Research Pub Date : 2023-11-07 DOI: 10.1155/2023/9439536

Zhaoxing Dong, Ting Li, Cenli Wang, Yong Zhou, Zhongkai Tong, Xuekui Du

{"title":"Sestrin2 Regulates Endoplasmic Reticulum Stress-Dependent Ferroptosis to Engage Pulmonary Fibrosis by Nuclear Factor Erythroid 2-Related Factor 2/Activating Transcription Factor 4 (NRF2/ATF4)","authors":"Zhaoxing Dong, Ting Li, Cenli Wang, Yong Zhou, Zhongkai Tong, Xuekui Du","doi":"10.1155/2023/9439536","DOIUrl":"https://doi.org/10.1155/2023/9439536","url":null,"abstract":"Pulmonary fibrosis (PF) can lead to chronic inflammation, the destruction of alveoli and irreversible lung damage. Sestrin2 is a highly protective stress-inducible protein that is involved in the cell response to various stress factors and the regulation of homeostasis and has a certain protective effect against PF. In this study, TGF-β1 was used to establish a PF cell model. Bleomycin was used to induce PF in mice, and the expression levels of related proteins were detected by western blotting. The levels of the inflammatory cytokine, TNF-α, IL-6, and IL-1β were detected by enzyme-linked immunosorbent assays. Immunoprecipitation was used to verify the interaction between ATF4 and NRF2 and between Sestrin2 and NRF2 to explore the specific mechanism by which Sestrin2 affects PF. The results showed that Sestrin2 inhibited fibroblast-to-myofibroblast transition (FMT), improved inflammation, promoted cell proliferation, and alleviated PF. Activating transcription factor 4/nuclear factor erythroid 2-related factor 2 (NRF2/ATF4) signaling pathway activation could alleviate endoplasmic reticulum stress, inhibit ferroptosis and FMT, and reduce reactive oxygen species levels, thereby alleviating PF. Overexpression of ATF4 and the addition of a ferroptosis inducer reversed Sestrin2-mediated alleviation of PF. In conclusion, Sestrin2 alleviates PF and endoplasmic reticulum stress-dependent ferroptosis through the NRF2/ATF4 pathway.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"69 6","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135433758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

GPC3 Promotes Lung Squamous Cell Carcinoma Progression and HLA-A2-Restricted GPC3 Antigenic Peptide-Modified Dendritic Cell-Induced Cytotoxic T Lymphocytes to Kill Lung Squamous Cell Carcinoma Cells. GPC3促进肺鳞状细胞癌进展和hla - a2限制性GPC3抗原肽修饰的树突状细胞诱导的细胞毒性T淋巴细胞杀死肺鳞状细胞癌细胞。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-11-06 eCollection Date: 2023-01-01 DOI: 10.1155/2023/5532617

Jing Ning, Jianqiao Ding, Shu Wang, Youhong Jiang, Daqing Wang, Shenyi Jiang

{"title":"GPC3 Promotes Lung Squamous Cell Carcinoma Progression and HLA-A2-Restricted GPC3 Antigenic Peptide-Modified Dendritic Cell-Induced Cytotoxic T Lymphocytes to Kill Lung Squamous Cell Carcinoma Cells.","authors":"Jing Ning, Jianqiao Ding, Shu Wang, Youhong Jiang, Daqing Wang, Shenyi Jiang","doi":"10.1155/2023/5532617","DOIUrl":"10.1155/2023/5532617","url":null,"abstract":"Lung squamous cell carcinoma (LUSC) is associated with poor clinical prognosis and lacks available targeted agents. GPC3 is upregulated in LUSC. Our study aimed to explore the roles of GPC3 in LUSC and the antitumor effects of HLA-A2-restricted GPC3 antigenic peptide-sensitized dendritic cell (DC)-induced cytotoxic T lymphocytes (CTLs) on LUSC. LUSC cells with GPC3 knockdown and overexpression were built using lentivirus packaging, and cell viability, clone formation, apoptosis, cycle, migration, and invasion were determined. Western blotting was used to detect the expression of cell cycle-related proteins and PI3K-AKT pathway-associated proteins. Subsequently, HLA-A2-restricted GPC3 antigenic peptides were predicted and synthesized by bioinformatic databases, and DCs were induced and cultured in vitro. Finally, HLA-A2-restricted GPC3 antigenic peptide-modified DCs were co-cultured with T cells to generate specific CTLs, and the killing effects of different CTLs on LUSC cells were studied. A series of cell function experiments showed that GPC3 overexpression promoted the proliferation, migration, and invasion of LUSC cells, inhibited their apoptosis, increased the number of cells in S phase, and reduced the cells in G2/M phase. GPC3 knockdown downregulated cyclin A, c-Myc, and PI3K, upregulated E2F1, and decreased the pAKT/AKT level. Three HLA-A2-restricted GPC3 antigenic peptides were synthesized, with GPC3522-530 FLAELAYDL and GPC3102-110 FLIIQNAAV antigenic peptide-modified DCs inducing CTL production, and exhibiting strong targeted killing ability in LUSC cells at 80 : 1 multiplicity of infection. GPC3 may advance the onset and progression of LUSC, and GPC3522-530 FLAELAYDL and GPC3102-110 FLIIQNAAV antigenic peptide-loaded DC-induced CTLs have a superior killing ability against LUSC cells.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"5532617"},"PeriodicalIF":4.1,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"107591453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Common Pollen Modulate Immune Responses against Viral-Like Challenges in Airway Coculture Model. 普通花粉调节气道共培养模型对病毒样挑战的免疫反应。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-11-06 eCollection Date: 2023-01-01 DOI: 10.1155/2023/6639092

Tarleena Tossavainen, Maria-Viola Martikainen, Hanna Loukola, Marjut Roponen

{"title":"Common Pollen Modulate Immune Responses against Viral-Like Challenges in Airway Coculture Model.","authors":"Tarleena Tossavainen, Maria-Viola Martikainen, Hanna Loukola, Marjut Roponen","doi":"10.1155/2023/6639092","DOIUrl":"10.1155/2023/6639092","url":null,"abstract":"Recent research indicates that exposure to pollen increases the risk and severity of respiratory infections, while studies also suggest that it may possess a protective function. Our aim was to investigate how exposure to common pollen modifies airway cells' responses to viral- or bacterial-like challenges and vice versa. Cocultured A549 and THP-1 cells were exposed to three doses of four different pollens (Alnus glutinosa, Betula pendula, Phleum pratense, or Ambrosia artemisiifolia) and subsequently to Toll-like receptor (TLR) ligands mimicking bacterial and viral challenges (TLR3, TLR4, TLR7/8). The stimulation experiment was replicated in reverse order. Toxicological and immunological end points were analyzed. When cells were primed with pollen, especially with grass (P. pratense) or weed (A. artemisiifolia), the ability of cells to secrete cytokines in response to bacterial- and viral-like exposure was decreased. In contrast, cells primed with viral ligand TLR7/8 showed greater cytokine responses against pollen than cells exposed to ligands or pollen alone. Our results suggest that pollen exposure potentially weakens immune reactions to bacterial- or viral-like challenges by modulating cytokine production. They also indicate that TLR7/8-mediated viral challenges could elicit exaggerated immune responses against pollen. Both mechanisms could contribute to the acceleration and complication of infections during the pollen season.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"6639092"},"PeriodicalIF":4.1,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"107591452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Understanding How Minerals Contribute to Optimal Immune Function. 了解矿物质如何促进最佳免疫功能。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-11-01 eCollection Date: 2023-01-01 DOI: 10.1155/2023/3355733

Alina Stefanache, Ionut-Iulian Lungu, Ioan-Adrian Butnariu, Gabriela Calin, Cristian Gutu, Constantin Marcu, Carmen Grierosu, Elena Roxana Bogdan Goroftei, Letitia-Doina Duceac, Marius Gabriel Dabija, Florina Popa, Daniela Damir

{"title":"Understanding How Minerals Contribute to Optimal Immune Function.","authors":"Alina Stefanache, Ionut-Iulian Lungu, Ioan-Adrian Butnariu, Gabriela Calin, Cristian Gutu, Constantin Marcu, Carmen Grierosu, Elena Roxana Bogdan Goroftei, Letitia-Doina Duceac, Marius Gabriel Dabija, Florina Popa, Daniela Damir","doi":"10.1155/2023/3355733","DOIUrl":"10.1155/2023/3355733","url":null,"abstract":"Sufficient mineral supply is vital not only for the innate immune system but also for the components of the adaptive immune defense, which encompass defense mechanisms against pathogens and the delicate balance of pro- and anti-inflammatory regulation in the long term. Generally, a well-balanced diet is capable of providing the necessary minerals to support the immune system. Nevertheless, specific vulnerable populations should be cautious about obtaining adequate amounts of minerals such as magnesium, zinc, copper, iron, and selenium. Inadequate levels of these minerals can temporarily impair immune competence and disrupt the long-term regulation of systemic inflammation. Therefore, comprehending the mechanisms and sources of these minerals is crucial. In exceptional circumstances, mineral deficiencies may necessitate supplementation; however, excessive intake of supplements can have adverse effects on the immune system and should be avoided. Consequently, any supplementation should be approved by medical professionals and administered in recommended doses. This review emphasizes the crucial significance of minerals in promoting optimal functioning of the immune system. It investigates the indispensable minerals required for immune system function and the regulation of inflammation. Moreover, it delves into the significance of maintaining an optimized intake of minerals from a nutritional standpoint.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"3355733"},"PeriodicalIF":4.1,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10632063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72014454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bone Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Ameliorated Lipopolysaccharide-Induced Lung Injury Via the miR-21-5p/PCSK6 Pathway. 骨间充质干细胞衍生的小细胞外小泡通过miR-21-5p/PCSK6途径改善脂多糖诱导的肺损伤。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-10-28 eCollection Date: 2023-01-01 DOI: 10.1155/2023/3291137

Bo Cai, Weidong Song, Song Chen, Jie Sun, Rui Zhou, Zhen Han, Jian Wan

{"title":"Bone Mesenchymal Stem Cell-Derived Small Extracellular Vesicles Ameliorated Lipopolysaccharide-Induced Lung Injury Via the miR-21-5p/PCSK6 Pathway.","authors":"Bo Cai, Weidong Song, Song Chen, Jie Sun, Rui Zhou, Zhen Han, Jian Wan","doi":"10.1155/2023/3291137","DOIUrl":"10.1155/2023/3291137","url":null,"abstract":"Acute lung injury (ALI) is a life-threatening disease that currently lacks a cure. Although stem cell-derived small extracellular vesicles (sEVs) have shown promising effects in the treatment of ALI, their underlying mechanisms and responsible components have yet to be identified. Proprotein convertase subtilisin/kexin type 6 (PCSK6) is a gene involved in inflammation and a potential target of miR-21-5p, a microRNA enriched in stem cell-derived sEVs. The current study investigated the role of PCSK6 in lipopolysaccharide (LPS)-induced ALI and its interaction with miR-21-5p. Notably, our results showed that PCSK6 expression was positively correlated with LPS stimulation. Knockdown of PCSK6 ameliorated LPS-induced inhibition of proliferation and upregulation of permeability in human BEAS-2B cells, whereas PCSK6 overexpression displayed the opposite effects. BEAS-2B cells were able to actively internalize the cocultured bone mesenchymal stem cell (MSC)-derived sEVs (BMSC-sEVs), which alleviated the cell damage caused by LPS. Overexpressing PCSK6, however, eliminated the therapeutic effects of BMSC-sEV coculture. Mechanistically, BMSC-sEVs inhibited PCSK6 expression via the delivery of miR-21-5p, which is directly bound to the PCSK6 gene. Our work provides evidence for the role of PCSK6 in LPS-induced ALI and identified miR-21-5p as a component of BMSC-derived sEVs that suppressed PCSK6 expression and ameliorated LPS-induced cell damage. These results reveal a novel molecular mechanism for ALI pathogenesis and highlight the therapeutic potential of using sEVs released by stem cells to deliver miR-21-5p for ALI treatment.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"3291137"},"PeriodicalIF":4.1,"publicationDate":"2023-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10626970/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71482351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tim-3 Is Differentially Expressed during Cell Activation and Interacts with the LSP-1 Protein in Human Macrophages. Tim-3在细胞激活过程中差异表达，并与人巨噬细胞中的LSP-1蛋白相互作用。

IF 4.1 3区医学

Journal of Immunology Research Pub Date : 2023-10-26 eCollection Date: 2023-01-01 DOI: 10.1155/2023/3577334

Ranferi Ocaña-Guzman, Lucero A Ramon-Luing, Luis A Vazquez-Bolaños, Michelle Rodríguez-Alvarado, Fausi Bulhusen-Rodriguez, Alonso Torres-Hatem, Karen Gonzalez-Torres, Mariana Citlalli de Alba-Alvarado, Isabel Sada-Ovalle

{"title":"Tim-3 Is Differentially Expressed during Cell Activation and Interacts with the LSP-1 Protein in Human Macrophages.","authors":"Ranferi Ocaña-Guzman, Lucero A Ramon-Luing, Luis A Vazquez-Bolaños, Michelle Rodríguez-Alvarado, Fausi Bulhusen-Rodriguez, Alonso Torres-Hatem, Karen Gonzalez-Torres, Mariana Citlalli de Alba-Alvarado, Isabel Sada-Ovalle","doi":"10.1155/2023/3577334","DOIUrl":"10.1155/2023/3577334","url":null,"abstract":"T-cell Immunoglobulin and Mucin Domain 3 (TIM-3) is an immune checkpoint receptor known to regulate T-cell activation and has been targeted for immunotherapy in cancer and other diseases. However, its expression and function in other cell types, such as macrophages, are poorly understood. This study investigated TIM-3 expression in human macrophages polarized to M1 (stimulated with IFN-γ and LPS) and M2 (stimulated with IL-4 and IL-13) phenotypes using an in vitro model. Our results show that M1 macrophages have a lower frequency of TIM-3+ cells compared to M2 macrophages at 48 and 72 hr poststimulation. Additionally, we observed differential levels of soluble ADAM 10, an enzyme responsible for TIM-3 release, in the supernatants of M1 and M2 macrophages at 72 hr. We also found that the TIM-3 intracellular tail might associate with lymphocyte-specific protein 1 (LSP-1), a protein implicated in cell motility and podosome formation. These findings enhance our understanding of TIM-3 function in myeloid cells such as macrophages and may inform the development of immunotherapies with reduced immune-related adverse effects.","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2023 ","pages":"3577334"},"PeriodicalIF":4.1,"publicationDate":"2023-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10622183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71482353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0