Carmen Garrido

ORCID: 0000-0003-1368-1493
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About
Contact & Profiles
Research Areas
  • Heat shock proteins research
  • Endoplasmic Reticulum Stress and Disease
  • Cell death mechanisms and regulation
  • HIV Research and Treatment
  • HIV/AIDS drug development and treatment
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Extracellular vesicles in disease
  • CAR-T cell therapy research
  • Cancer-related Molecular Pathways
  • Acute Lymphoblastic Leukemia research
  • Ubiquitin and proteasome pathways
  • RNA Interference and Gene Delivery
  • Autophagy in Disease and Therapy
  • DNA Repair Mechanisms
  • HIV/AIDS Research and Interventions
  • Toxin Mechanisms and Immunotoxins
  • Cancer therapeutics and mechanisms
  • thermodynamics and calorimetric analyses
  • Lung Cancer Treatments and Mutations
  • Cancer Immunotherapy and Biomarkers
  • Erythrocyte Function and Pathophysiology
  • Immune Cell Function and Interaction
  • ATP Synthase and ATPases Research
  • Connexins and lens biology
  • Hemoglobinopathies and Related Disorders

Inserm
2016-2025

Université de Bourgogne
2016-2025

Centre Georges François Leclerc
2016-2025

La Ligue Contre le Cancer
2015-2025

CHU Dijon Bourgogne
1994-2025

Universidad Nacional Autónoma de México
2025

Centre de recherche Translationnelle en Médecine moléculaire
2014-2024

Laboratoire de Recherche Vasculaire Translationnelle
2024

Hospital Universitario Son Espases
2015-2024

Université Bourgogne Franche-Comté
2016-2023

Systemic anticancer chemotherapy is immunosuppressive and mostly induces nonimmunogenic tumor cell death. Here, we show that even in the absence of any adjuvant, cells dying response to anthracyclins can elicit an effective antitumor immune suppresses growth inoculated tumors or leads regression established neoplasia. Although both antracyclins mitomycin C induced apoptosis with caspase activation, only anthracyclin-induced immunogenic death was immunogenic. Caspase inhibition by Z-VAD-fmk...

10.1084/jem.20050915 article EN The Journal of Experimental Medicine 2005-12-19

Myeloid-derived suppressor cells (MDSCs) have been identified in humans and mice as a population of immature myeloid with the ability to suppress T cell activation. They accumulate tumor-bearing shown contribute cancer development. Here, we isolated tumor-derived exosomes (TDEs) from mouse lines that an interaction between TDE-associated Hsp72 MDSCs determines suppressive activity via activation Stat3. In addition, soluble factors triggered MDSC expansion Erk. Stat3 TLR2/MyD88-dependent...

10.1172/jci40483 article EN Journal of Clinical Investigation 2010-01-19

We investigated the mechanisms of immune tolerance raised by tumors comparing immunogenic and tolerogenic tumor cell clones isolated from a rat colon carcinoma. When injected into syngeneichosts, REGb cells yield that are rejected, while PROb progressive inhibit regression tumors. show here volume is correlated with an expansion CD4(+)CD25(+) regulatory T lymphocytes in lymphoid tissues. These delay vivo rejection vitro cell-mediated responses against through mechanism requires contact...

10.1002/eji.200324181 article EN European Journal of Immunology 2004-02-01

We have previously shown that the small heat shock protein HSP27 inhibited apoptotic pathways triggered by a variety of stimuli in mammalian cells. The present study demonstrates overexpression decreases U937 human leukemic cell sensitivity to etoposide-induced cytotoxicity preventing apoptosis. As observed for Bcl-2, delays poly(ADP-ribose)polymerase cleavage and procaspase-3 activation. In contrast with does not prevent cytochrome c release from mitochondria. cell-free system, addition...

10.1096/fasebj.13.14.2061 article EN The FASEB Journal 1999-11-01

A cellular defense mechanism counteracts the deleterious effects of misfolded protein accumulation by eliciting a stress response. The cytoplasmic deacetylase HDAC6 (histone 6) was previously shown to be key element in this response coordinating clearance aggregates through aggresome formation and their autophagic degradation. Here, for first time, we demonstrate that is involved another crucial cell ubiquitinated aggregates, unravel its molecular basis. Indeed, our data show senses...

10.1101/gad.436407 article EN Genes & Development 2007-09-01

In the era of immunotherapies there is an urgent need to implement use circulating biomarkers in clinical practice facilitate personalized therapy and predict treatment response. We conducted a prospective study evaluate usefulness exosomal-PD-L1 melanoma patients' follow-up. studied dynamics from 100 patients by using enzyme-linked immunosorbent assay. found that PD-L1 was secreted through exosomes cells. Exosomes carrying had immunosuppressive properties since they were as efficient cancer...

10.1080/20013078.2019.1710899 article EN Journal of Extracellular Vesicles 2020-01-07

Exosomes, via heat shock protein 70 (HSP70) expressed in their membrane, are able to interact with the toll-like receptor 2 (TLR2) on myeloid-derived suppressive cells (MDSCs), thereby activating them. We analyzed exosomes from mouse (C57Bl/6) and breast, lung, ovarian cancer patient samples cultured different approaches, including nanoparticle tracking analysis, biolayer interferometry, FACS, electron microscopy. Data were Student's t Mann-Whitney tests. All statistical tests two-sided....

10.1093/jnci/djv330 article EN JNCI Journal of the National Cancer Institute 2015-11-22

The cysteine proteases known as caspases play a central role in most apoptotic pathways. Here, we show that caspase inhibitors arrest the maturation of human erythroid progenitors at early stages differentiation, before nucleus and chromatin condensation. Effector such caspase-3 are transiently activated through mitochondrial pathway during erythroblast differentiation cleave proteins involved integrity (lamin B) condensation (acinus) without inducing cell death cleavage GATA-1. These...

10.1084/jem.193.2.247 article EN The Journal of Experimental Medicine 2001-01-15
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