Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Objective: Obesity is a major risk factor for atherosclerosis and is associated with increased cardiovascular morbidity and mortality. However, the precise molecular pathways responsible for this close association remain poorly understood.
Methods And Results: In this study, we report that leptin-deficiency (ob/ob) in low-density lipoprotein receptor knockout (ldlr(-/-)) mice induces an unexpected 2.2- to 6-fold reduction in atherosclerotic lesion development, compared with ldlr(-/-) mice having similar total cholesterol levels. Ldlr(-/-)/ob/ob mice show reduced T cell helper type 1 (Th1) response, enhanced expression of Foxp3, the specification transcription factor of regulatory T (Treg) cells, and improved Treg cell function. Leptin receptor-deficient (db/db) mice display marked increase in the number and suppressive function of Treg cells. Supplementation of Treg-deficient lymphocytes with Treg cells from db/db mice in an experimental model of atherosclerosis induces a significant reduction of lesion size and a marked inhibition of interferon (INF)-gamma production, compared with supplementation by Treg cells from wild-type mice.
Conclusions: These results identify a critical role for leptin/leptin receptor pathway in the modulation of the regulatory immune response in atherosclerosis, and suggest that alteration in regulatory immunity may predispose obese individuals to atherosclerosis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1161/ATVBAHA.107.149567 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Maternal-Fetal Interface Cell Dysfunction in Patients With Preeclampsia Revealed via Single-Cell RNA Sequencing.
Am J Reprod Immunol
September 2025
Department of Obstetrics and Gynecology, Second XiangYa Hospital of Central South University, Changsha, Hunan, China.
Problem: Preeclampsia (PE) is a leading cause of perinatal maternal and fetal mortality. Clinical and pathological studies suggest that placental and decidual cell dysfunction may contribute to this condition. However, the pathogenesis of PE remains poorly understood.
View Article and Find Full Text PDFSalmonella-superspreader hosts require gut regulatory T cells to maintain a disease-tolerant state.
J Exp Med
November 2025
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.
Host-pathogen interactions involve two critical strategies: resistance, whereby hosts clear invading microbes, and tolerance, whereby hosts carry high pathogen burden asymptomatically. Here, we investigate mechanisms by which Salmonella-superspreader (SSP) hosts maintain an asymptomatic state during chronic infection. We found that regulatory T cells (Tregs) are essential for this disease-tolerant state, limiting intestinal immunopathology and enabling SSP hosts to thrive, while facilitating Salmonella transmission.
View Article and Find Full Text PDFImpact of Serum/Xeno-Free Medium and Cytokine Supplementation on CAR-T Cell Therapy Manufacturing in Stirred Tank Bioreactors.
Biotechnol J
September 2025
Department of Biochemical Engineering, University College London, London, UK.
Chimeric antigen receptor T-cell (CAR-T) therapies have demonstrated clinical efficacy in treating haematological malignancies, resulting in multiple regulatory approvals. However, there is a need for robust manufacturing platforms and the use of GMP-aligned reagents to meet the clinical and commercial demands. This study investigates the impact of serum/xeno-free medium (SXFM) and cytokine supplementation on CAR-T cell production in static and agitated culture systems, using 24-well plate G-Rex vessels and 500 mL stirred tank bioreactors (STRs), respectively.
View Article and Find Full Text PDFIntestinal epithelial Ceacam1 deficiency prevents steroid-refractory acute gut graft-versus-host disease.
JCI Insight
September 2025
Arthur D. Riggs Diabetes and Metabolism Research Institute, The Beckman Research Institute, and.
Steroid-refractory gut acute graft-versus-host disease (SR-Gut-aGVHD) is the major cause of nonrelapse death after allogeneic hematopoietic cell transplantation. High numbers of donor-type IL-22+ T cells, IL-22-dependent dysbiosis, and loss of antiinflammatory CX3CR1hi mononuclear phagocytes (MNPs) play critical roles in SR-Gut-aGVHD pathogenesis. CEACAM1 on intestinal epithelial cells (IECs) is proposed to regulate bacterial translocation and subsequent immune responses in the intestine.
View Article and Find Full Text PDFRestoration of the lamina propria duodenal immune infiltrate in gluten-free diet treated coeliac patients despite persistent villous atrophy.
Clin Exp Immunol
September 2025
Mucosal Immunology Lab, Department of Paediatrics and Immunology. Universidad de Valladolid. Valladolid. Spain.
Introduction: Although Coeliac disease (CD) current and only treatment is a life-long strict gluten free diet (GFD), some patients suffer from persistent duodenal lesions despite years into the diet. Hence, we aimed to study the effect that the GFD elicits on the mucosal immune infiltrate from these patients.
Method: To that end, duodenal biopsies were collected from non-coeliac controls and CD patients, both at diagnosis and after at least one year into the GFD.