Critical Reviews in Immunology最新文献_第7页

microRNA-99b regulates Bacillus Calmette-Guerin-infected immature dendritic cell-induced CD4 T cell differentiation by targeting mTOR signaling microRNA-99b通过靶向mTOR信号通路调控calmette - guerin感染的未成熟树突状细胞诱导的CD4 T细胞分化

4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/critrevimmunol.2023050312

Libo Zhen, Yuanyuan Chen, Juwei Gao, Boying Li, Yangmin Jia

{"title":"microRNA-99b regulates Bacillus Calmette-Guerin-infected immature dendritic cell-induced CD4 T cell differentiation by targeting mTOR signaling","authors":"Libo Zhen, Yuanyuan Chen, Juwei Gao, Boying Li, Yangmin Jia","doi":"10.1615/critrevimmunol.2023050312","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2023050312","url":null,"abstract":"Objective: This study aimed to elucidate the mechanisms by which microRNA-99b (miR-99b) regulates CD4 T cell differentiation induced by Bacillus Calmette-Guerin (BCG)-infected immature dendritic cells (imDCs). Methods: BCG-infected imDCs were employed to induce CD4 T cell differentiation. Levels of miR-99b, interferon-gamma (IFN-γ), Foxp3, interleukin (IL)-10, IL-17, IL-23, and ROR-γt were assessed. Effects of miR-99b inhibition and mechanistic target of rapamycin (mTOR) agonist on Th17/Treg cell ratio and cytokine levels (IL-6, IL-17, IL-23) were studied. Expression of mTOR, S6K1, and 4E-BP1 related to miR-99b was analyzed. Results: BCG-infected imDCs led to CD4 T cell differentiation and altered levels of IFN-γ, Foxp3, IL-10, miR-99b, IL-17, IL-23, and ROR-γt. Inhibition of miR-99b increased the Th17/Treg cell ratio in CD4 T cells co-cultured with BCG-infected imDCs, and this effect was further enhanced by the mTOR agonist. Additionally, the miR-99b inhibitor elevated the levels of IL-6, IL-17, and IL-23 when CD4 T cells were co-cultured with BCG-infected imDCs, and the mTOR agonist further amplified this increase. Notably, miR-99b negatively regulated mTOR signaling, as the miR-99b inhibitor upregulated the expression levels of mTOR, S6K1, and 4E-BP1 while decreasing miR-99b. Conclusion: miR-99b modulates CD4 T cell differentiation via mTOR pathway in response to BCG-infected imDCs. Inhibiting miR-99b affects Th17/Treg ratio and pro-inflammatory cytokines, potentially impacting tuberculosis immunotherapies.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135267404","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

Interleukin 34 in Disease Progressions: A Comprehensive Review. 白细胞介素34在疾病进展中的作用：综述。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023050326

Prerona Boruah, Nikhita Deka

引用次数: 0

Recent Advancement and Novel Application of Natural Polyphenols for the Treatment of Allergy Asthma: From Phytochemistry to Biological Implications. 天然多酚治疗过敏性哮喘的最新进展和新应用：从植物化学到生物学意义。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023050289

Meera Kumari, Mohd Aftab Siddiqui, Amresh Gupta

{"title":"Recent Advancement and Novel Application of Natural Polyphenols for the Treatment of Allergy Asthma: From Phytochemistry to Biological Implications.","authors":"Meera Kumari, Mohd Aftab Siddiqui, Amresh Gupta","doi":"10.1615/CritRevImmunol.2023050289","DOIUrl":"10.1615/CritRevImmunol.2023050289","url":null,"abstract":"Allergic diseases, primarily IgE-mediated, exert a substantial global health burden. A pivotal role in allergic reactions is played by mast cells, with histamine serving as a central mediator. Within this context, plant-based polyphenols, abundantly present in vegetables and fruits, show promising potential for allergy prevention. These natural compounds, particularly flavonoids, possess anti-inflammatory and anti-allergic properties, influencing dendritic cells, modulating macrophages, and fostering the proliferation of B cells and T cells. The potent anti-allergic effects of flavonoids are attributed to their ability to reduce the production of signaling factors, suppress cytokine production, and regulate signal transduction and gene expression in mast cells, basophils, and T cells. Notably, their benefits extend beyond allergy prevention, as they hold promise in the prevention and treatment of autoimmune illnesses such as diabetes, rheumatoid arthritis, and multiple sclerosis. In the context of allergic reactions and autoimmune diseases, polyphenols exhibit immunomodulatory effects by inhibiting autoimmune T cell proliferation and downregulating pro-inflammatory cytokines. In recent times, flavonoids, being the most prevalent polyphenols in food, have garnered significant attention from researchers due to their potential health advantages. This review compiles the latest scientific research to highlight the impact of flavonoids on allergic illnesses and their potential as a beneficial dietary component.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 4","pages":"29-41"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220750","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: 1

Physical Activity Increases Immunity to COVID-19 Infection. 体育活动增强对新冠肺炎感染的免疫力。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023049460

Kiran Dudhat

{"title":"Physical Activity Increases Immunity to COVID-19 Infection.","authors":"Kiran Dudhat","doi":"10.1615/CritRevImmunol.2023049460","DOIUrl":"10.1615/CritRevImmunol.2023049460","url":null,"abstract":"Coronavirus are truly one of the maximum critical fantastic-stranded non-segmented RNA viruses, named after the approximately 126-nm-diameter envelope around the nucleic acid-protein complicated. The virus causes significant harm to human fitness, including direct injury to the respiratory system, immune system compromise, worsening of the underlying clinical conditions, and eventually systemic failure and death. Exercise affects the immune system's antiviral mechanisms. Modest exercise, done before or after infection, improves morbidity and mortality to the contamination, according to animal investigations using influenza and simplex virus in the respiratory tract. Moreover, preclinical research has demonstrated that overtraining has a negative impact on the body's response to viral infections. Follow-up research has shed some light on the mechanisms underlying these discoveries. Through the activation of muscle protein synthesis, physical activity (PA) and exercise are essential for maintaining muscle mass. On the other hand, a lack of muscle contractile activity throughout the country of no exercise, particularly in elderly people, is a major contributor to anabolic rigidity and muscle atrophy.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 5","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220752","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

Th17 Cells: Orchestrators of Mucosal Inflammation and Potential Therapeutic Targets. Th17细胞：粘膜炎症的协调因子和潜在的治疗靶点。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023050360

Dorsa Iraji, Bergithe E Oftedal, Anette S B Wolff

{"title":"Th17 Cells: Orchestrators of Mucosal Inflammation and Potential Therapeutic Targets.","authors":"Dorsa Iraji, Bergithe E Oftedal, Anette S B Wolff","doi":"10.1615/CritRevImmunol.2023050360","DOIUrl":"10.1615/CritRevImmunol.2023050360","url":null,"abstract":"T helper 17 (Th17) cells represent a specialized subgroup of effector CD4+ T cells known for their role in provoking neutrophil-driven tissue inflammation, particularly within mucosal tissues. Although they are pivotal for defending the host against extracellular bacteria and fungi, they have also been associated with development of various T cell-mediated inflammatory conditions, autoimmune diseases, and even cancer. Notably, Th17 cells exhibit a dual nature, with different Th17 cell subtypes showcasing distinct effector functions and varying capacities to incite autoimmune tissue inflammation. Furthermore, Th17 cells exhibit significant plasticity, which carries important functional implications, both in terms of their expression of cytokines typically associated with other effector T cell subsets and in their interactions with regulatory CD4+ T cells. The intricate balance of Th17 cytokines can also be a double-edged sword in inflammation, autoimmunity, and cancer. Within this article, we delve into the mechanisms that govern the differentiation, function, and adaptability of Th17 cells. We culminate with an exploration of therapeutic potentials in harnessing the power of Th17 cells and their cytokines. Targeted interventions to modulate Th17 responses are emerging as promising strategies for autoimmunity, inflammation, and cancer treatment. By precisely fine-tuning Th17-related pathways, we may unlock new avenues for personalized therapeutic approaches, aiming to restore immune balance, alleviate the challenges of these disorders, and ultimately enhance the quality of life for individuals affected by them.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 5","pages":"25-52"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220753","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

Silencing of FUN14 domain containing 1 inhibits platelet activation in diabetes mellitus through blocking mitophagy 含1的FUN14结构域的沉默通过阻断线粒体自噬抑制糖尿病血小板活化

4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/critrevimmunol.2023050364

Qiang Wu, Siwen Yu, Kangkang Peng

{"title":"Silencing of FUN14 domain containing 1 inhibits platelet activation in diabetes mellitus through blocking mitophagy","authors":"Qiang Wu, Siwen Yu, Kangkang Peng","doi":"10.1615/critrevimmunol.2023050364","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2023050364","url":null,"abstract":"Objectives: Platelet hyperactivity is an adverse physiological event in diabetes mellitus (DM). This study aimed to explore the function of FUN14 domain containing 1 (FUNDC1) on the platelet activation in DM and reveal relevant mechanisms involving mitophagy. Methods: A mouse model of DM was established by high fat feeding and streptozotocin injection. Platelets that separated from whole blood were incubated with FCCP to induce mitophagy. Relative mRNA expression of FUNDC1 was detected by qRT-PCR. The protein expression of FUNDC1, LC3-II/LC3-I, FUNDC1 (two mitophagy marker), and cleaved caspase-3 (a pro-apoptotic factor) were measured by western blot. Immunofluorescence and flow cytometry were performed to detect LC3-positive mitochondria and CD62P (a platelet activating factor), respectively. Besides, the serum levels of β-TG and PF4 (two platelet specific proteins) were measured by enzyme linked immunosorbent assay. Results: FUNDC1 is up-regulated in DM mice, and its silencing decreased the body weight and fasting blood glucose. Silencing of FUNDC1 also significantly weakened the effects of FCCP on inducing platelet mitophagy, evidenced by the down-regulation of LC3-II/LC3-I, up-regulation of Tomm20, and a decrease in LC3-positive mitochondria. In addition, the platelets were activated in DM mice. Silencing of FUNDC1 weakened platelet hyperactivity in DM, evidenced by the down-regulation of cleaved caspase-3 and CD62P, and the decrease in β-TG and PF4 levels. Conclusions: Silencing of FUNDC1 inhibits platelet hyperactivity in DM through blocking mitophagy. FUNDC1-midiated mitophagy may be a promising target for the treatment of DM and related cardiovascul","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"102 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135319415","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

4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/critrevimmunol.2023051091

Kawaljit Kaur, Anahid Jewett

引用次数: 0

Plausible Role of NLRP3 Inflammasome and Associated Cytokines in Pathogenesis of Rheumatic Heart Disease. NLRP3炎症小体和相关细胞因子在类风湿性心脏病发病机制中的合理作用。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023049463

Aishwarya Rani, Devinder Toor

{"title":"Plausible Role of NLRP3 Inflammasome and Associated Cytokines in Pathogenesis of Rheumatic Heart Disease.","authors":"Aishwarya Rani, Devinder Toor","doi":"10.1615/CritRevImmunol.2023049463","DOIUrl":"10.1615/CritRevImmunol.2023049463","url":null,"abstract":"Rheumatic heart disease (RHD) is a post-streptococcal sequela caused by Streptococcus pyogenes. The global burden of disease is high among people with low socio-economic status, with significant cases emerging every year despite global eradication efforts. The current treatment includes antibiotic therapies to target strep throat and rheumatic fever and valve replacement strategies as a corrective measure for chronic RHD patients. Valvular damage and valve calcification are considered to be the end-stage processes of the disease resulting from impairment of the endothelial arrangement due to immune infiltration. This immune infiltration is mediated by a cascade of events involving NLRP3 inflammasome activation. NLRP3 inflammasome is activated by wide range of stimuli including bacterial cell wall components like M proteins and leukocidal toxins like nicotinamide dehydrogenase (NADase) and streptolysin O (SLO) and these play a major role in sustaining the virulence of Streptococcus pyogenes and progression of RHD. In this review, we are discussing NLRP3 inflammasome and its plausible role in the pathogenesis of RHD by exploiting the host-pathogen interaction mainly focusing on the NLRP3 inflammasome-mediated cytokines IL-1β and IL-18. Different therapeutic approaches involving NLRP3 inflammasome inactivation, caspase-1 inhibition, and blockade of IL-1β and IL-18 are discussed in this review and may be promising for treating RHD patients.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 3","pages":"1-14"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220745","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

Identification of Potential Targets and Mechanisms of Sinomenine in Allergic Rhinitis Treatment Based on Network Pharmacology and Molecular Docking. 基于网络药理学和分子对接的青藤碱治疗过敏性鼻炎的潜在靶点和机制鉴定。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023049479

Xuemei Liu, Hong Chen, Xiaobo Chen, Peng Wu, Jianhua Zhang

{"title":"Identification of Potential Targets and Mechanisms of Sinomenine in Allergic Rhinitis Treatment Based on Network Pharmacology and Molecular Docking.","authors":"Xuemei Liu, Hong Chen, Xiaobo Chen, Peng Wu, Jianhua Zhang","doi":"10.1615/CritRevImmunol.2023049479","DOIUrl":"10.1615/CritRevImmunol.2023049479","url":null,"abstract":"This study aimed to investigate the potential targets and molecular mechanism of sinomenine in treating allergic rhinitis (AR) using network pharmacology and molecular docking. Relevant targets of sinomenine and AR were obtained from public databases, and differentially expressed genes (DEGs) for AR were identified in the Gene Expression Omnibus database. Using VennDiagram, we identified 22 potential targets of sinomenine against AR by crossing disease targets, drug targets, and DEGs. Functional analysis revealed that sinomenine may act via its anti-inflammatory and immunosuppressive effects, and its action pathways may include the MAPK, HIF-1, and JAK-STAT pathways. Furthermore, hub targets were identified using EPC, MCC, and MNC algorithms, and six hub targets (STAT3, EGFR, NFKB1, HIF1A, PTGS2, and JAK1) were selected by integrating the top 10 hub genes and 22 potential targets. Molecular docking analysis indicated that STAT3, EGFR, PTGS2, and JAK1 may be key targets of sinomenine against AR. Overall, our results suggest that sinomenine has potential therapeutic effects against AR, and its mechanism of action may involve the regulation of key targets and pathways related to inflammation and immunity.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 4","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220747","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

KIAA1429 Promotes Nasopharyngeal Carcinoma Progression by Mediating m6A Modification of PTGS2. KIAA1429通过介导PTGS2的m6A修饰促进鼻咽癌的进展。

IF 1.3 4区医学

Critical Reviews in Immunology Pub Date : 2023-01-01 DOI: 10.1615/CritRevImmunol.2023050249

Lingling Wu, Yuanhong Zhou, Jun Fu

{"title":"KIAA1429 Promotes Nasopharyngeal Carcinoma Progression by Mediating m6A Modification of PTGS2.","authors":"Lingling Wu, Yuanhong Zhou, Jun Fu","doi":"10.1615/CritRevImmunol.2023050249","DOIUrl":"10.1615/CritRevImmunol.2023050249","url":null,"abstract":"Emerging evidence suggests that dysregulation of a N6-methyladenosine (m6A) methyltransferase KIAA1429 participates in the pathogenesis of multiple cancers except for nasopharyngeal carcinoma (NPC). This study is aimed to explore the function of KIAA1429 in NPC progression. The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets were used to confirm the mRNA expression in NPC by bioinformatic analysis. The levels of KIAA1429 and PTGS2 was detected by quantitative reverse transcription polymerase chain reaction and Western blotting. To investigate the effects of KIAA1429/PTGS2 knockdown or overexpression vectors on NPC cell malignancy, cell and animal experiments were performed. Finally, MeRIP and mRNA stability assays were used to verify the m6A modification and mRNA stability, respectively. KIAA1429 was upregulated in NPC tissues and cells. After transfecting KIAA1429 knockdown or overexpression vectors in NPC cells, we proved that KIAA1429 overexpression promoted proliferation, migration, invasion, and tumor growth, whereas KIAA1429 knockdown showed the opposite effect. Our results also indicated that KIAA1429 mediated m6A modification of PTGS2, enhancing PTGS2 mRNA stability in NPC cells. In addition, PTGS2 could also regulate the effects of KIAA1429 on NPC cell malignancy. This study confirmed the oncogenic function of KIAA1429 in NPC through m6A-modification of PTGS2, suggesting that targeting KIAA1429-mediated m6A modification of PTGS2 might provide a new therapeutic strategy for NPC.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"43 4","pages":"15-27"},"PeriodicalIF":1.3,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41220748","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