Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Regulatory T cells (Tregs) are physiologically designed to prevent autoimmune disease and maintain self-tolerance. In tumour microenvironments, their presence is related to a poor prognosis, and they influence the therapeutic outcome due to their capacity to suppress the immune response by cell-cell contact and to release immunosuppressive cytokines. In this study, we demonstrate that Treg immunosuppressive activity can be modulated by the cross-linking between the CD45RA expressed by Tregs and the C-type lectin MGL. This specific interaction strongly decreases the immunosuppressive activity of Tregs, restoring the proliferative capacity of co-cultured T lymphocytes. This effect can be attributed to changes in CD45RA and TCR signalling through the inhibition of Lck and inactivation of Zap-70, an increase in the Foxp3 methylation status and, ultimately, the reduced production of suppressive cytokines. These results indicate a role of MGL as an immunomodulator within the tumour microenvironment interfering with Treg functions, suggesting its possible use in the design of anticancer vaccines.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493043 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0132617 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
Potential Impact of Extracorporeal Photopheresis on Trained Immunity and Organ Transplant Acceptance.
Transplant Direct
September 2025
Unidad Transplante de О́rganos, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain.
Extracorporeal photopheresis (ECP) is a well-established, safe, and effective immunomodulatory therapy currently used in clinics to decrease T cell-mediated immunity in various disorders, including autoimmune diseases and chronic rejection in organ transplantation. Although the ECP procedure has been shown to induce apoptotic cells that are reintroduced into the patient at the end of the treatment, the precise tolerogenic mechanisms mediated by ECP are not fully understood. Previous in vitro studies have demonstrated that early apoptotic cells express annexins on their cell surface, which suppress myeloid cell activation on stimulation with bacterial lipopolysaccharide through Toll-like receptors.
View Article and Find Full Text PDFDendritic Cells Induce Clec5a-mediated Immune Modulation in MPTP-induced Parkinson's Disease Mouse Model.
Front Biosci (Landmark Ed)
August 2025
Division of Life Sciences and Department of Life Science, Graduate School, CHA University, 13488 Seongnam-si, Gyeonggi-do, Republic of Korea.
Background: Parkinson's disease (PD) is characterized by a progressive decline in dopaminergic neurons within the substantia nigra (SN). Although its underlying cause has yet to be fully elucidated, accumulating evidence suggests that neuroinflammation contributes substantially to disease development. Treatment strategies targeting neuroinflammation could improve PD outcomes.
View Article and Find Full Text PDFEstrogen Receptor-α Loss Accelerates Cartilage Degradation through CLEC3B-Mediated Chondrocyte Hypertrophy and Inflammation.
Osteoarthritis Cartilage
September 2025
Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh Swanson School of Engineering, Pittsburgh, PA, USA; Orland Bethel Family Musculoskeletal Research Center, University of Pittsburgh School of Med
Objective: Previous studies in our lab demonstrated that estrogen receptor-α (ERα) levels in cartilage decreased with osteoarthritis (OA). We also defined the essential role of ERα in maintaining the health of chondrocytes. However, most of the studies were conducted in vitro, and the physiological link between ERα loss and cartilage degradation has not been demonstrated using animal models.
View Article and Find Full Text PDFRole of mTORC1 signaling in postnatal microglia activation preceding neurodegeneration in a mouse model for Niemann-Pick disease Type C.
PLoS One
September 2025
Department of Biology, Providence College, Providence, Rhode Island, United States of America.
In Npc1 deficient mice, postnatal developmental alterations in cerebellar microglia and Purkinje cells (PCs) are followed by early-onset neurodegeneration. Even in the absence of PC loss, microglia in Npc1nmf164 mice display hallmark features of activation during early postnatal development, including increased proliferation, enhanced phagocytic activity, and morphological changes indicative of an activated state. In this study, we investigated whether mammalian target of rapamycin complex 1 (mTORC1) drives postnatal activation of cerebellar microglia in Npc1nmf164 mice.
View Article and Find Full Text PDFThe severity of influenza is often driven by an excessive host immune response rather than the virus itself, yet the key molecular drivers within specific immune cells remain poorly understood. While recent single-cell RNA sequencing studies have successfully identified immune populations involved, they have largely not identified the upstream drivers modulating their pro-inflammatory functions. Here we employed an integrated single-cell co-expression network to address this gap.
View Article and Find Full Text PDF