A5080502438- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cytomegalovirus and herpesvirus research
- Telomeres, Telomerase, and Senescence
- Immunotherapy and Immune Responses
- Immune cells in cancer
- Nanoplatforms for cancer theranostics
- interferon and immune responses
- Advanced biosensing and bioanalysis techniques
- Skin Protection and Aging
- Cancer Immunotherapy and Biomarkers
- Circadian rhythm and melatonin
- Heme Oxygenase-1 and Carbon Monoxide
- Immune Cell Function and Interaction
- High Altitude and Hypoxia
- Genomics and Chromatin Dynamics
- Toxoplasma gondii Research Studies
- Inflammatory mediators and NSAID effects
- Eicosanoids and Hypertension Pharmacology
- PARP inhibition in cancer therapy
- Spectroscopy and Quantum Chemical Studies
- Autophagy in Disease and Therapy
- Calcium signaling and nucleotide metabolism
- DNA Repair Mechanisms
- Genetics, Aging, and Longevity in Model Organisms
- Breastfeeding Practices and Influences
Institute for Research in Biomedicine
2019-2024
Institute of Science and Technology
2022
Universidad Pablo de Olavide
2020
Centro Andaluz de Biología Molecular y Medicina Regenerativa
2020
Universidad de Sevilla
2005-2020
Universitat de València
2009
Universidad Cardenal Herrera CEU
2009
McGill University
2008
Abstract Chemotherapy often generates intratumoral senescent cancer cells that strongly modify the tumor microenvironment, favoring immunosuppression and growth. We discovered, through an unbiased proteomics screen, immune checkpoint inhibitor programmed cell death 1 ligand 2 (PD-L2) is highly upregulated upon induction of senescence in different types cells. PD-L2 not required for to undergo senescence, but it critical evade system persist intratumorally. Indeed, after chemotherapy,...
Abstract Senescent cells accumulate in tissues over time, favoring the onset and progression of multiple age‐related diseases. present a remarkable increase lysosomal mass elevated autophagic activity. Here, we report that two main pathways macroautophagy (MA) chaperone‐mediated autophagy (CMA) are constitutively upregulated senescent cells. Proteomic analyses subpopulations lysosomes preferentially engaged each these types revealed profound quantitative qualitative changes cells, affecting...
Recent reports in oncological and non-oncological experimental setups provide strong evidence that senescent cells are under the surveillance of CD8 T cell-mediated adaptive immunity. These new data also shed light on mechanisms sensitize to cell-dependent killing, as well those enable evade cell immunosurveillance. Understanding interplay between cellular senescence immune system may open strategies ameliorate aging aging-associated diseases.
The objective was to analyze variations in dental arch width relation oral habits. Maxillary and mandibular intercanine intermolar distance were determined certain habits 1297 children (ages 3 6 years). After an examination, the parents of each child completed a questionnaire about habits, including use dummy or bottle (or both), finger sucking, mouth breathing, breast- bottle-feeding, duration these Data subjected statistical analysis by chi-square test for qualitative variables variance...
Cancer therapy often induces senescence in some cancer cells. Senescent cells, due to their profoundly altered biology, may conceivably interact with the adaptive immune system novel ways that boost immunosurveillance, triggering clearance of both senescent and non-senescent neoplastic In this regard, we have recently reported cells exhibit potent antigenicity adjuvanticity can elicit strong CD8+ T cell-dependent anticancer effects when used as vaccination agents.
Abstract Anti-cancer therapies often result in a subset of surviving cancer cells that undergo therapy-induced senescence (TIS). Senescent strongly modify the intratumoural microenvironment favoring immunosuppression and, thereby, tumour growth. An emerging strategy to optimise current is combine them with treatments eliminate senescent cells. To this end, we undertook an unbiased proteomics approach identify surface markers contributing immune evasion. Through approach, discovered...
ABSTRACT Cellular senescence is a stress response that activates innate immunity. However, the interplay between senescent cells and adaptive immune system remains largely unexplored. Here, we show display enhanced MHC class I (MHC-I) antigen processing presentation. Immunization of mice with syngeneic fibroblasts generates CD8 T reactive against both normal fibroblasts, some them targeting senescence-associated MHC-I-peptides. In context cancer, demonstrate cancer trigger strong anti-tumor...
The repair of DNA breaks takes place in the context chromatin and thus involves activity remodelers. nucleosome acetyltransferase H4 (NuA4) remodeler complex enables break by relaxing flanking chromatin. Here, we show that MRG domain binding protein (MRGBP), a member this complex, acts as general inhibitor double-strand repair. Upon its downregulation, is generally increased. This particularly evident for stimulation early events homologous recombination. Thus, MRGBP has an opposing role to...
<div>Abstract<p>Cellular senescence is a stress response that activates innate immune cells, but little known about its interplay with the adaptive system. Here, we show senescent cells combine several features render them highly efficient in activating dendritic (DC) and antigen-specific CD8 T cells. This includes release of alarmins, activation IFN signaling, enhanced MHC class I machinery, presentation senescence-associated self-peptides can activate In context cancer,...
<p>Senescent cancer cells activate dendritic cells</p>
<p>Senescent cells upregulate MHC-I antigen presentation</p>
<p>Senescent cancer cells from human patients hyperstimulate autologous reactive TILs</p>
<p>Noncancer senescent cells induce an adaptive immune response in vivo and present unique immunogenic peptides</p>
<p>Senescent cancer cells from human patients hyperstimulate autologous reactive TILs</p>