Sébastien Jacquelin

ORCID: 0000-0001-5087-3641
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Acute Myeloid Leukemia Research
  • Immune Cell Function and Interaction
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Immune cells in cancer
  • Immunotherapy and Immune Responses
  • Epigenetics and DNA Methylation
  • Chemokine receptors and signaling
  • Complement system in diseases
  • Cell Adhesion Molecules Research
  • Hematopoietic Stem Cell Transplantation
  • Angiogenesis and VEGF in Cancer
  • Eosinophilic Disorders and Syndromes
  • Advanced biosensing and bioanalysis techniques
  • Protein Degradation and Inhibitors
  • Kruppel-like factors research
  • CRISPR and Genetic Engineering
  • Chronic Myeloid Leukemia Treatments
  • Cancer-related molecular mechanisms research
  • Congenital heart defects research
  • Histone Deacetylase Inhibitors Research
  • Cancer Immunotherapy and Biomarkers
  • RNA modifications and cancer
  • Renal and related cancers
  • Immune Response and Inflammation
  • Autophagy in Disease and Therapy

The University of Queensland
2023-2025

Mater Research
2022-2024

QIMR Berghofer Medical Research Institute
2015-2024

Translational Research Institute
2023-2024

Inserm
2013-2023

Université Paris Cité
2009-2023

Institut des Maladies Génétiques Imagine
2023

Sorbonne Université
2013

Assistance Publique – Hôpitaux de Paris
2009-2013

Pitié-Salpêtrière Hospital
2013

Critical immune-suppressive pathways beyond programmed death 1 (PD-1) and ligand (PD-L1) require greater attention. Nectins nectin-like molecules might be promising targets for immunotherapy, since they play critical roles in cell proliferation migration exert immunomodulatory functions pathophysiological conditions. Here, we show CD155 expression both malignant cells tumor-infiltrating myeloid humans mice. Cd155–/– mice displayed reduced tumor growth metastasis via DNAM-1 upregulation...

10.1172/jci98769 article EN Journal of Clinical Investigation 2018-05-13

Long noncoding RNAs (lncRNAs) have surpassed the number of protein-coding genes, yet majority no known function. We previously discovered 844 lncRNAs that were genetically linked to breast cancer through genome-wide association studies (GWAS). Here, we show a subset these alter risk by modulating cell proliferation, and provide evidence reduced expression on one lncRNA increases aberrant DNA replication repair.

10.1186/s12943-024-02021-y article EN cc-by Molecular Cancer 2024-05-15

Abstract Treg are immune cells that play a critical role in the regulation of response. Although transcription factor Foxp3 is widely accepted as standard marker Treg, specific surface markers needed to better characterize these and decipher their mechanisms action. Neuropilin‐1 (Nrp‐1), membrane protein primarily involved nervous system, was identified murine but its expression has not been rigorously investigated human Treg. Here we show contrast regardless origins (blood, thymus, spleen,...

10.1002/eji.200839040 article EN European Journal of Immunology 2009-06-01

Chemotherapy enhances the antitumor adaptive immune T cell response, but immunosuppressive tumor environment often dominates, resulting in cancer relapse. Antigen-presenting cells such as tumor-associated macrophages (TAMs) and dendritic (TuDCs) are main protagonists of tumor-infiltrating lymphocyte (TIL) immuno-suppression. TAMs have been widely investigated associated with poor prognosis, immuno-suppressive activity TuDCs is less well understood. We performed two-photon imaging tissue to...

10.1593/neo.121572 article EN cc-by-nc-nd Neoplasia 2013-01-01

Germ-line deletion of a conserved enhancer (the Fms intrinsic regulatory element, FIRE) in the mouse Csf1r locus causes congenital absence microglia. Homozygous FIRE on C57BL/6J background leads to perinatal lethality and hydrocephalus (HC) surviving pups. We developed congenic line with defined regions non-C57BL/6J genomic DNA, increased postnatal viability reduced incidence HC. Both HC were eliminated F2 mice following outcross CBA/J or BALBc/J backgrounds. To assess impacts microglial...

10.1101/2025.01.16.633478 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2025-01-17

Abstract Acute myeloid leukemia (AML) is a genetically heterogeneous, aggressive hematological malignancy induced by distinct oncogenic driver mutations. The effect of specific AML oncogenes on immune activation or suppression unclear. Here, we examine responses in models and demonstrate that dictate immunogenicity, the quality response escape through immunoediting. Specifically, expression Nras G12D alone sufficient to drive potent anti-leukemia increased MHC Class II can be overcome with...

10.1038/s41467-023-37592-9 article EN cc-by Nature Communications 2023-04-14

Regenerative capabilities of the endothelium rely on vessel-resident progenitors termed endothelial colony forming cells (ECFCs). This study aimed to investigate if these are impacted by conditions (i.e., obesity or atherosclerosis) characterized increased serum levels oxidized low-density lipoprotein (oxLDL), a known inducer Endothelial-to-Mesenchymal Transition (EndMT). Our investigation focused understanding effects EndMT self-renewal and associated molecular alterations. In presence...

10.1007/s10456-024-09927-7 article EN cc-by Angiogenesis 2024-05-11

Abstract The caudal-related homeobox transcription factor CDX2 is expressed in leukemic cells but not during normal blood formation. Retroviral overexpression of Cdx2 induces AML mice, however the developmental stage at which exerts its effect unknown. We developed a conditionally inducible mouse model to determine effects vivo, expression hematopoietic stem and progenitor (HSPCs). Cdx2-transgenic mice develop myelodysplastic syndrome with progression acute leukemia associated acquisition...

10.1038/s41467-020-16840-2 article EN cc-by Nature Communications 2020-06-15

Complement activation has shown a role in murine models of graft-versus-host disease (GVHD) and endothelial complications after allogeneic hematopoietic cell transplantation (allo-HSCT). However, its impact on post-transplant outcomes not been so far fully elucidated. Here, we conducted prospective multicentric trial (NCT01520623) performing serial measurements complement proteins, regulators, CH50 activity for 12 weeks allo-HSCT 85 patients receiving myeloablative conditioning (MAC) regimen...

10.1002/ajh.27030 article EN cc-by-nc American Journal of Hematology 2023-07-22

ABSTRACT Long noncoding RNAs (lncRNAs) have surpassed the number of protein-coding genes, yet majority no known function. We previously discovered >800 lncRNAs at regions identified by breast cancer genome-wide association studies (GWAS). Here, we performed a pooled CRISPR-Cas13d RNA knockdown screen to identify which these altered cell proliferation. found that KILR, lncRNA functions as tumor suppressor, safeguards cells against uncontrolled The half-life KILR is significantly reduced...

10.1101/2023.11.16.567471 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-11-17

The upregulation of inhibitory molecules is a major driver immune escape in cancer. In contrast, less known about the regulation T cell activating receptors within tumor microenvironment. Here, we describe that derived CD155, transmembrane glycoprotein immunoglobulin superfamily, downregulates receptor CD226 (DNAM-1) mouse and human CD8+ cells, leading to profound loss effector function cancer evasion. Mechanistically, CD155 drives internalisation through phosphorylation tyrosine 319...

10.2139/ssrn.3466329 article EN SSRN Electronic Journal 2019-01-01
Coming Soon ...