A5018358278- Lymphoma Diagnosis and Treatment
- Viral-associated cancers and disorders
- Immune Cell Function and Interaction
- Chronic Lymphocytic Leukemia Research
- Cytomegalovirus and herpesvirus research
- T-cell and Retrovirus Studies
- NF-κB Signaling Pathways
- Immunodeficiency and Autoimmune Disorders
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Monoclonal and Polyclonal Antibodies Research
- Cancer Immunotherapy and Biomarkers
- Eosinophilic Disorders and Syndromes
- CAR-T cell therapy research
- Histiocytic Disorders and Treatments
- Lung Cancer Research Studies
- Herpesvirus Infections and Treatments
- Cancer, Hypoxia, and Metabolism
- Autoimmune and Inflammatory Disorders
- Toxin Mechanisms and Immunotoxins
- Glycosylation and Glycoproteins Research
- RNA regulation and disease
- Biomedical Ethics and Regulation
- Acute Myeloid Leukemia Research
- Cancer-related Molecular Pathways
Université de Limoges
2010-2024
Centre National de la Recherche Scientifique
2009-2023
Contrôle de la Réponse Immune B et Lymphoproliférations
2009-2023
Inserm
2002-2023
Centre National pour la Recherche Scientifique et Technique (CNRST)
2023
Hôpital Dupuytren
2010-2021
Hôpital Universitaire Dupuytren
2009-2017
Centre Hospitalier Universitaire de Limoges
2016
Institut National de Recherche en Santé Publique
2009
Université Toulouse III - Paul Sabatier
2007-2009
The Epstein-Barr virus (EBV) latency III program imposed by EBNA2 and LMP1 is directly responsible for immortalization of B cells in vitro thought to mediate most immunodeficiency-related posttransplant lymphoproliferative diseases vivo. To answer the question whether how this proliferation related c-Myc, we have established transcriptome both c-Myc EBV programs using a Lymphochip specialized microarray. In addition EBV-positive I Burkitt lymphoma lines lymphoblastoid cell (LCLs), used an...
EBV-immortalized B cells induce a complex immune response such that the virus persists as clinically silent infection for lifetime of infected host. B7-H1, also called PD-L1, is cosignaling molecule B7 family can inhibit activated T cell effectors by interaction with its receptor PD-1. In this work, we have studied dependence B7-H1 on NF-κB and c-Myc, two main transcription factors in EBV latency III proliferating cells, various lymphoblastoid Burkitt lymphoma lines, some them being...
Diffuse large B-cell lymphoma (DLBCL) is a fatal malignancy that needs to identify new targets for additional therapeutic options. This study aimed clarify the clinical and biological significance of endogenous neurotrophin (nerve growth factor (NGF) brain-derived neurotrophic (BDNF)) in DLBCL biopsy samples cell lines. We analysed expression NGF, BDNF, their receptors (Trk, p75NTR) 51 biopsies lines by immunohistochemistry, immunofluorescence, western blotting. To investigate role...
While c-Myc dysregulation is constantly associated with highly proliferating B-cell tumors, nuclear factor (NF)-κB addiction found in indolent lymphomas as well diffuse large lymphomas, either an activated like phenotype or the Epstein-Barr virus. We raised question of effect B cells NF-κB by three different inducers: virus-latency III program, TLR9 and CD40. Induction overexpression increased proliferation immortalized cells, that was dependent on NF-κB. Results from transcriptomic...
Escape from immune control must be important in the natural course of B-cell lymphomas, especially for those with activation NF-κB. The pre-clinical LMP1/CD40-expressing transgenic mouse model is characterized by specific CD40 signaling responsible NF-κB continuous a spleen monoclonal tumor after 1 year 60% cases. LMP1/CD40 tumors B-cells expressed high levels PD-L1. This expression was dependent on either NF-κB, JAK1/JAK2 or BTK pathways since these were activated and ex vivo treatment...
ABSTRACT Epstein-Barr virus (EBV) classically infects and transforms B lymphocytes in vitro, yielding lymphoblastoid cell lines (LCLs). In contrast to other herpesviruses, EBV is not described as an infectious agent for monocytes. However, recent papers vitro infection of monocytes leading abortive or transient viral expression. the present study, we report characterization E1, a monocytic line infected transformed by EBV. This was derived from LCL drastic electroporation selection...
We examined lymph nodes and tonsils from patients with infectious mononucleosis by combined detection of EBV-encoded RNA a specific marker natural killer (NK) cells, PEN5. A small number Epstein-Barr virus (EBV) latently infected nonneoplastic NK cells were detected. Our data demonstrate that are targets EBV infection these is an early event observed during primary infection.
Abstract EBV infects and immortalizes B cells in vitro vivo. It is the causative agent of most immune deficiency–related lymphoproliferative disorders associated with various lymphomas. latency III–transformed are known to express two immunosuppressive molecules, IL-10 PD-L1, characteristics regulatory (Bregs). In this study, we show that, addition secretion Breg cytokines IL-10, IL-35, TGF-β1, were able repress proliferation their autologous T preactivated by CD2, CD3, CD28. This inhibitory...
Activating mutations of MYD88 (MYD88L265P being the far most frequent) are found in cases Waldenström macroglobulinemia (WM) as well various aggressive B-cell lymphoma entities with features plasma cell (PC) differentiation, such activated type diffuse large (DLBCL). To understand how activation exerts its transformation potential, we developed a new mouse model which MYD88L252P protein, murine ortholog human MYD88L265P, is continuously expressed CD19 positive B-cells together Yellow...
Overexpression and activation of TPM3-ALK tyrosine kinase fusion protein is a causal oncogenic event in the development Anaplastic Large Cell Lymphoma Inflammatory Myofibroblastic ALK-positive tumors. Thus, ALK specific inhibitors current therapeutic challenge. Animal models are essential to assess, vivo, efficiency ALK-oncogene identify new and/or additional targets tumorigenesis pathway. Using tetracycline system allow conditional concomitant luciferase expression, we have developed unique...
Chronic lymphocytic leukemia (CLL) is an incurable indolent non-Hodgkin lymphoma characterized by tumor B cells that weakly express a B-cell receptor. The mutational status of the variable region (IGHV) within immunoglobulin heavy chain (IGH) locus important prognosis indicator and raises question CLL cell origin. Mutated IGHV gene are genetically imprinted activation-induced cytidine deaminase (AID). AID also required for IGH rearrangements: class switch recombination between Mu (Sμ) 3’...
Relationships between c-Rel and GCB-DLBCLs remain unclear. We found that strong DNA-binding activity was mostly in GCBs on two independent series of 48 DLBCLs 66 DLBCLs, the latter issued from GHEDI series. associated with increased REL mRNA expression. Extending study to whole Lenz DLBCL published 202 233 cases, it gene expression profile (GEP) overlapped partially (12%) but only GCB GEP not ABC-DLBCLs. Cases both overexpression were defined as those having a signature. These cases 88 83%...
Epstein–Barr virus (EBV) is associated with Hodgkin’s disease (HD). However, EBV-positive Reed–Sternberg (RS) cells and B lymphocytes co-exist in the same lymph node affected by HD. In a previous report, using total DNA, presence of two distinct EBV strains was demonstrated, but their cellular localization (i.e. RS vs lymphocytes) could not be determined. To address this question, three patients EBV-associated HD were selected present study single-cell PCR latent membrane protein-1 ( LMP-1 )...
Background In Epstein-Barr virus-associated Hodgkin's lymphomas, neoplastic Reed-Sternberg cells and surrounding non-tumor B-cells contain different variants of the LMP1-BNLF1 oncogene. this study, we raised question functional properties latent membrane protein 1 (LMP1) natural from both B-cells.Design Methods Twelve LMP1 cells, lymphomas benign reactive lymph nodes were cloned, sequenced stably transfected in murine recombinant interleukin-3-dependent Ba/F3 to search for relationships...
The repair DNA polymerase beta (Polbeta), when overexpressed, plays a critical role in generating genetic instability via its interference with the genomic replication program. Up-regulation of Polbeta has been reported many tumor types that exhibit aberrations, including EBV-related B-cell lymphomas. However, mechanisms responsible for overexpression have never examined. Here, we report both expression and activity Polbeta, EBV-immortalized B cells, are induced by several natural variants...
<title>Abstract</title> The Sµ-3'RR recombination (Sµ-3'RRrec) in B cells, a genomic rearrangement occurring within the immunoglobulin heavy chain (IGH) locus is believed to lead cell receptor (BCR) loss. Its increased frequency patients with chronic lymphocytic leukemia (CLL), especially those high <italic>MYC</italic> expression, suggests c-MYC contribute genetic instability during oncogenesis To explore c-MYC's role enhancing Sµ-3'RRrec, study used λ-c-MYC transgenic (Tg) mouse model...
While studying c-Myc protein expression in several Burkitt lymphoma cell lines and lymph nodes from a mouse model bearing translocated c-MYC gene the human BL line IARC-BL60, we surprisingly discovered complex electrophoretic profile. Indeed, BL60 carrying t(8;22) translocation exhibits simple pattern, with single c-Myc2 isoform. Analysis of transcripts expressed by tumor λc-MYC (Avy/a) showed for first time five that are associated translocation. The were correlated production c-MycS, loss...
Abstract Here, we created a conditional transgenic mouse model with insertion of sequence coding for both MYD88 L252P and the Yellow Fluorescent Protein (YFP) into rosa26 -locus. B-cell specific induction transgene constantly led to spleen enlargement expansion YFP positive B-cells in 8-12 month-old mice, moderate proliferation increase. Being clonal or oligoclonal, these exhibited marked morphological immunophenotypic lymphoplasmocytic aspect plasma cell transcriptomic signature serum...