Critical Reviews in Immunology最新文献

{"title":"Neonatal Immunity to Candida: Current Understanding and Contributions of Murine Models.","authors":"Angel Palacios, Ajay Kumar, Fides Myles C Caliwag, Miguel A Becerril-Garcia","doi":"10.1615/CritRevImmunol.2024055053","DOIUrl":"10.1615/CritRevImmunol.2024055053","url":null,"abstract":"<p><p>Neonatal candidiasis poses significant clinical challenges due to its potential for severe morbidity and mortality in vulnerable infants. Due to their underdeveloped immune system, neonates are at a higher risk for infections caused by Candida species. They can vary from mild to severe, including penetrating deep tissues, bloodstream spread, and dissemination to organs. The immune system of newborns is marked by a limited innate immune response, with lower levels of pro-inflammatory cytokines. Adaptive immunity, important for lasting protection, also experiences delayed maturation with weakened Th1 and Th17 responses. These shortcomings result in a higher vulnerability to Candida infections during infancy. Murine models have been crucial in understanding the reasons behind this susceptibility. These models assist in examining how different immune elements, like neutrophils, macrophages, and T cells, and their interactions are involved in Candida infections. Moreover, they offer an understanding of how early-life exposure to Candida affects immune responses and may aid in developing possible therapeutic plans. In this article we review current results from research to provide a thorough summary and critical insights into neonatal immune response to Candida, highlighting the importance of using murine models in this field of study. Understanding these immune dynamics is essential for creating specific treatments and preventive strategies to prevent newborns from Candida infections, ultimately improving neonatal health outcomes.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"63-76"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460860","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}

{"title":"Study of TNF-α, IFN-γ, IL-10, TGF-β and IL-6 Gene Polymorphisms in a Cohort of Professionals Who Worked in the First Pandemic Wave in the Brazilian Amazon.","authors":"Beatriz Dos Reis Marcelino, Marcelo Cleyton da Silva Vieira, Marcos Jessé Abrahão Silva, Lilian Cristina Santos Sinfronio da Silva, Ellen Polyana da Costa Gurrão, Everaldina Cordeiro Dos Santos, Jeanne Gonçalves Cabral, Alex Brito Souza, Daniele Melo Sardinha, Rebecca Lobato Marinho, Sebastião Kauã de Sousa Bispo, Karla Valéria Batista Lima, Luana Nepomuceno Gondim Costa Lima","doi":"10.1615/CritRevImmunol.2024055001","DOIUrl":"10.1615/CritRevImmunol.2024055001","url":null,"abstract":"<p><p>Genetic polymorphisms in genes that enable the production of an effective host immune response, such as single nucleotide polymorphisms (SNPS) in the IL-6, INF-alpha, IFN-gamma, IL-10, TGF-beta genes can cause unfavorable clinical conditions or susceptibility to pathologies. The objective of this work is to evaluate the epidemiological and genetic profile of professionals from health institutions during the first pandemic wave. A case-control study was performed with convenience sampling from health institutions (HI) workers from Belém-PA, Northern Brazil (N = 213), divided into symptomatology groups (Asymptomatic-AS, n = 91; and Symptomatic-SI, n = 122); and severity groups classified by chest computerized tomography-CCT data (symptomatic with pulmonary involvement-SCP, n = 37; symptomatic without pulmonary involvement-SSP, n = 8). Genotyping was performed by sanger sequencing for SNP TNF-α -308 G/A (rs1800629), IFN-γ +874 T/A (rs2430561), TGF-β codon 10 (rs1982073), codon 25 (rs1800471), IL-6 - 174 G/C (rs180079), IL-10 - 1082 A/T (rs1800896), -819 C/T (rs1800871), and -592 A/C (rs1800872), and statistical analysis through the Epilfo program. Significant association was observed between the presence of comorbidities and poor prognosis of COVID-19 (especially between COVID-19 and overweight and obesity). Only the TNF-α 308 G/A snp was significantly associated with the symptoms and severity of COVID-19. These findings about this TNF-α SNP passed in the multiple testing correction at a false discovery rate (FDR)< 0.05. These data can help medicine and the scientific community understand the influence of genetics and epidemiological parameters in combating COVID-19.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"39-61"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460861","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}

{"title":"miR-205-5p Promotes the Proliferation, Migration, and Invasion of Nasopharyngeal Carcinoma Cells by Regulating CALM1.","authors":"Zhengdong Guo, Hongming Zhu, Renmin Zhang, Qiang Shan, Yajing Wang","doi":"10.1615/CritRevImmunol.2024055296","DOIUrl":"10.1615/CritRevImmunol.2024055296","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC), a malignant tumor originating from the epithelium and glands. MicroRNAs (miRNAs) play an essential role in the tumorigenesis and metastasis of NPC. They are effective biomarkers in the detection of malignant progression of NPC. In this study, we analyzed the expression profiles of miRNAs in NPC patients with Gene Expression Omnibus (GEO) database. ceRNA networks of NPC were constructed and target miRNAs were screened. MTT, colony formation and Transwell experiments were used to explore the effects of miR-205-5p on the proliferation, migration and invasion ability of NPC cells. Bioinformatics analysis combined with Double luciferase experiment verified the binding relationship between miR-205-5p and CALM1. We identified 34 long non-coding RNAs (lncRNAs), 22 miRNAs, and 145 messenger RNAs (mRNAs) and constructed a competing endogenous RNAs (ceRNA) network to explain the relationship between RNA expression profiles and NPC progression. Of which, we found that 5 miRNAs (hsa-let-7d-5p, hsa-let-7e-5p, hsa-let-7f-5p, hsa-miR-143-3p and hsa-miR-205-5p) are related to clinical features. We further found that miR-205-5p was highly expressed in NPC cell lines. In addition, MTT, colony formation and Transwell assays showed that miR-205-5p promoted the proliferation, migration and invasion of NPC cells. Double luciferase detection showed that miR-205-5p could target combined with CALM1. In addition, we found that miR-205-5p could promote the proliferation, migration and invasion of NPC cells by inhibited the expression of CALM1. Overall, the present study demonstrated that as a carcinogenic factor, miR-205-5p can affect the malignant progression of NPC by mediating CALM1.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"25-38"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460859","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}

{"title":"The Overexpression of EP4 Attenuates the Killing Ability of CD8+ T Cells against Prostate Cancer Cells through the PI3K/AKT Signaling Pathway.","authors":"Ying Zhou, Lanying Zou, Jun Xu, Xiaoping Zhou, Huichuan Zhao","doi":"10.1615/CritRevImmunol.2024052115","DOIUrl":"10.1615/CritRevImmunol.2024052115","url":null,"abstract":"<p><p>Immunotherapy has shown significant promise in the clinical management of prostate cancer (PCa), and prostaglandin E receptor 4 (EP4) is a key governing factor in PCa progression. However, the molecular mechanisms by which EP4 influences immunotherapy in PCa have yet to be elucidated. This investigation was designed to unravel the specific mechanisms through which EP4 affects the killing ability of CD8+ T cells against PCa cells. Immunohistochemistry was utilized to assay the expression of EP4, programmed death ligand 1 (PD-L1), and CD8+ T cell infiltration in tissue samples, and quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot (WB) were used to evaluate EP4 expression in cells. PCa cell lines with either EP4 knockdown or overexpression were co-cultured with CD8+ T cells. Lactase dehydrogenase toxicity assays were employed to measure CD8+T cell killing ability, and ELISA was employed to measure interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and interleukin-2 (IL-2) levels. Expression of T cell exhaustion markers was detected by flow cytometry. Rescue experiments were conducted utilizing 3-methyladenine [a phosphoinositide 3-kinase (PI3K) inhibitor] and PD-L1 knockdown. The impact of EP4 overexpression on the PI3K/AKT signaling pathway-mediated PD-L1 expression and its subsequent modulation of CD8+ T cell killing ability against PCa cells was assessed through qRT-PCR, WB, flow cytometry, and immunofluorescence. EP4 exhibited a substantial upregulation in both PCa tissues and cells, displaying a positive correlation with PD-L1 expression and a converse negative correlation with the infiltration of CD8+ T cells. Knockdown of EP4 expression inhibited CD8+ T cell exhaustion, enhanced CD8+ T cell killing ability against PCa cells, increased the levels of IFN-γ, IL-2, and TNF-α, and decreased PD-L1 expression. Conversely, EP4 overexpression resulted in opposite effects, but treatment with 3-methyladenine mitigated EP4-induced promotion of PD-L1, p-AKT, and t-AKT expression. Furthermore, the knockdown of PD-L1 mitigated the inhibitory impact of EP4 overexpression on the killing ability of CD8+ T cell and the levels of IFN-γ, IL-2, and TNF-α, all while leaving the expression of p-AKT and t-AKT unaffected. EP4 was significantly overexpressed in PCa and activated PD-L1 expression via the PI3K/AKT signaling pathway, thereby suppressing the activity of CD8+ T cells.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"1-13"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460869","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}

{"title":"Diagnostic Power of the CD4+/CD8+ Ratio and the Expression of Activation and Memory Markers in Differentiating Sarcoidosis from Tuberculosis, Idiopathic Pulmonary Fibrosis, and Other Interstitial Lung Diseases.","authors":"Sara El Fakihi, Aicha El Allam, Hicham Tahoune, Chaimae Kadi, Azeddine Ibrahimi, Jamal-Eddine Bourkadi, Fouad Seghrouchni","doi":"10.1615/CritRevImmunol.2025056518","DOIUrl":"10.1615/CritRevImmunol.2025056518","url":null,"abstract":"<p><strong>Background: </strong>Sarcoidosis is a complex inflammatory disease of unknown etiology affecting mostly the lungs and poses a significant diagnostic challenge, particularly in regions where tuberculosis (TB) is endemic. The diagnostic complexity intensifies due to shared clinical and radiological features between sarcoidosis and TB, as well as similarities with idiopathic pulmonary fibrosis (IPF) in cases that progress to pulmonary fibrosis. Accurately distinguishing between these diseases is critical for timely and effective patient management.</p><p><strong>Objective: </strong>This study breaks new ground by evaluating the diagnostic power of the bronchoalveolar lavage (BAL) CD4/ CD8 ratio, along with key activation and memory markers to differentiate sarcoidosis from TB, IPF, and other-interstitial lung diseases (ILDs).</p><p><strong>Methods: </strong>A cohort of 68 patients with ILDs, including sarcoidosis (n = 37), TB (n = 19), IPF (n = 6), and Other-ILDs (n = 6) were assessed. The CD4/CD8 ratio and a panel of activation and memory markers were analyzed through flow cytometry.</p><p><strong>Results: </strong>Sarcoidosis exhibited a significantly higher CD4/CD8 ratio compared to those with TB, IPF, and Other-ILDs. An optimal cutoff value of 3.7 for the CD4/CD8 ratio in sarcoidosis with an area under the ROC curve (AUC) of 0.7%, had a specificity of 96.8%, and a sensitivity of 43.2%. In addition, a significant difference was detected in CD38, CD45RA, CD45RO, and CD62L expression.</p><p><strong>Conclusion: </strong>Combining the CD4/CD8 ratio (> 3.7) with the expression of CD38, CD62L, and memory markers is a promising new tool for the differential diagnosis of sarcoidosis.</p>","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"45 2","pages":"77-89"},"PeriodicalIF":0.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460857","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}

{"title":"TREM2 in Regulating Macrophage Inflammatory Responses and Disease Pathogenesis","authors":"Milan Medd","doi":"10.1615/critrevimmunol.2024054889","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024054889","url":null,"abstract":"Triggering receptor expressed on myeloid cells 2 (TREM2) is a cell-surface receptor belonging to the TREM family that is predominantly expressed on myeloid cells such as granulocytes, monocytes, osteocytes, macrophages, and microglia. While much of the functionality of TREM2 is not well understood at the molecular level, it is well-established that TREM2 plays a significant role in the regulation of a broad definition of macrophage inflammatory responses. Dysregulation of TREM2 has been implicated in a large number of diseases including Alzheimer’s disease, Nasu-Hakola disease, bone-related diseases, and atherosclerosis. The TREM2 gene is highly conserved evolutionarily and at the level of controlling its expression. The function of TREM2 is highly conserved across the broad definition of macrophages, including microglia, osteoclasts, and vascular macrophages. This genetic and physiological “niche conservatism” strongly suggests its pivotal role in regulating inflammatory responses. This mini-review summarizes our current understanding of the structure, expression, and function of TREM2 in the pathogenesis of macrophage-mediated diseases.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"38 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142178419","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}

{"title":"Commentary: Ovarian cancer; path to effective treatments","authors":"Anahid Jewett, Sanaz Memarzadeh, Kawaljit Kaur","doi":"10.1615/critrevimmunol.2024053766","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024053766","url":null,"abstract":"Despite advancements in cancer therapeutics such as checkpoint inhibitors and some targeted therapies, we have not achieved success in effectively treating ovarian cancer, since these therapeutics only benefit a subset of patients, and also provide short-term protection or cure. The use of chemotherapy and radiation therapy can cause depletion and/or lack of immune cells’ function. CAR-T therapy is found effective against several blood-based cancers, but limited success was seen against solid tumors. Targeting fewer antigens and significant side effects of therapy decreases the efficacy of CAR-T cells as immunotherapeutic in solid tumors, even though there is a great drive and significant effort to establish these therapies around the world. Bispecific and tri-specific antibodies have recently been advocated as effective cancer therapeutics. However, these also suffer the fate of CAR-Ts since the loss of antigen on tumor cells will render these therapeutics ineffective. At the moment we should design therapeutics that may have synergistic effects on killing/treating tumors. The only way we can establish that will be by learning the mechanisms of actions of immune therapeutics. Thus, advancement in the knowledge and effective strategies are required to develop cancer immuno-therapeutics","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"100 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141253595","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}

{"title":"N6-methyladenosine (m6A) reader LRPPRC-mediated CXCL11 induces cell inflammation to drive breast cancer cell malignancy","authors":"Qing Li, Changchun Zhang, Li Li","doi":"10.1615/critrevimmunol.2024053166","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024053166","url":null,"abstract":"Background: Breast cancer (BC) is among the most prevalent malignant cancers in women. This paper proposed to investigate the function as well as the regulatory mechanism of N6-methyladenosine (m6A) reader leucine rich pentatricopeptide repeat containing (LRPPRC) in BC inflammation and progression.\u0000Methods: The levels of LRPPRC and C-X-C motif chemokine ligand 11 (CXCL11) were detected via qRT-PCR. The regulatory mechanisms between LRPPRC and CXCL11 were investigated by RIP, MeRIP, and mRNA stability experiments. Moreover, the bio-functions of LRPPRC and CXCL11 in BC cells were explored through the CCK8, wound healing, Transwell assays. ELISA was utilized to evaluate pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) levels.\u0000Results: LRPPRC had a considerably higher level in BC samples than in healthy samples, and LRPPRC overexpression predicted poor prognosis. LRPPRC lowexpression diminished BC cell viability, migration, and invasion, whereas overexpression facilitated malignancy. LRPPRC exerted its stimulative effect through CXCL11 m6A modification. CXCL11 upregulating suppressed the LRPPRC silencing’s antitumor effect on BC cells malignancy. CXCL11 upregulation enhances inflammatory factors secretion by BC cells.\u0000Conclusion: This study demonstrated that LRPPRC aggravated BC inflammation and malignancy by upregulating m6A modification of CXCL11. These findings offered a potential to be a target for BC patients’ therapy.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"153 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141505469","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}

{"title":"The SLE Conundrum: A Comprehensive Analysis of Pathogenesis, Re-cent Developments, and the Future of Therapeutic Interventions","authors":"Uddeshya Sharma","doi":"10.1615/critrevimmunol.2024053504","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024053504","url":null,"abstract":"Systemic Lupus Erythematosus (SLE) is a complex autoimmune disorder with multifactorial interactions among various susceptibility factors. Significant strides have been made in under-standing the pathogenesis of SLE, leading to the development of targeted therapies and the exploration of alternative treatments. The approval of new therapies has expanded patient treatment options, and ongoing clinical trials promise to enhance the treatment landscape fur-ther. The future of SLE treatment lies in personalized, targeted therapies that minimize side effects and improve patient outcomes. This review comprehensively analyzes SLE’s current and prospects based on recent studies, patents, clinical trials, and formulations. Continued research and clinical trials are crucial to uncovering new therapeutic options and ultimately transforming the treatment landscape for SLE. With sustained efforts and advancements in medical science, we can offer a better quality of life and improved survival rates for SLE pa-tients.","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"2016 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140805245","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}

{"title":"The effect of supplementation of vitamin D on hyperlipidemia and bone mass in the pediatric with obesity","authors":"Feifan Wang, Lingshan Bei, Xiaoyan Zhang, Yangxi Fu","doi":"10.1615/critrevimmunol.2024052129","DOIUrl":"https://doi.org/10.1615/critrevimmunol.2024052129","url":null,"abstract":"Objective\u0000Vitamin D deficiency is known to be a significant factor in metabolic diseases such as obesity and diabetes. However, there is currently a lack of evidence regarding the effects of vitamin D on hyperlipidemia, glucose metabolism, and bone mass in pediatric patients with obesity.\u0000Methods\u0000Our study aimed to determine the relationship between Serum 25(OH)D and metabolic syndrome, as well as investigate the effect of Vitamin D3 supplementation on hyperlipidemia, glucose metabolism, and bone mass in pediatric patients with obesity. We conducted a cross-sectional study between January 2018 and January 2020, with a total of 723 children invited to participate. Of these, 283 were in the supplemented group (SG) and 440 were in the placebo group (PG). We evaluated blood pressure, fasting glucose, high-density lipoprotein, total cholesterol, low-density lipoprotein, and bone mineral density (BMD) among all subjects.\u0000Results\u0000We found that cholesterol, triglyceride, and glucose levels were strongly associated with 25(OH)D3 levels at baseline. After vitamin D3 supplementation, we observed a significant increase in body mass index (BMI) (P=0.02) and serum 25(OH)D3(P&lt;0.01) levels in the vitamin D3 group compared to the placebo group. Additionally, serum lipids such as total cholesterol(P&lt;0.01), HDL-c(P&lt;0.01), Total cholesterol/HDL-c (P&lt;0.01), LDL-c/HDL-c (P&lt;0.01), Triglycerides/HDL-c(P&lt;0.01) were significantly decreased in the Vit D group compared to the placebo group. Serum 25(OH)D was inversely associated with cholesterol, triglycerides, and fasting glucose.\u0000Conclusion\u0000Our results suggest that vitamin D3 supplementation can enhance the beneficial effect of hyperlipi","PeriodicalId":55205,"journal":{"name":"Critical Reviews in Immunology","volume":"1 1","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140805052","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}