Lilian Roland

ORCID: 0000-0003-4079-1911
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • Lymphoma Diagnosis and Treatment
  • Chronic Lymphocytic Leukemia Research
  • Viral-associated cancers and disorders
  • Acute Myeloid Leukemia Research
  • Monoclonal and Polyclonal Antibodies Research
  • NF-κB Signaling Pathways
  • Cytomegalovirus and herpesvirus research
  • Chemokine receptors and signaling
  • Glycosylation and Glycoproteins Research
  • Cell Adhesion Molecules Research
  • Hematopoietic Stem Cell Transplantation
  • Otitis Media and Relapsing Polychondritis
  • T-cell and B-cell Immunology

Institut de recherche Saint-Louis
2023-2025

Inserm
2019-2025

Université Paris Cité
2023-2025

Hôpital Saint-Louis
2023-2025

Acute Leukemia French Association
2025

Centre National de la Recherche Scientifique
2019-2023

Contrôle de la Réponse Immune B et Lymphoproliférations
2018-2021

Université de Limoges
2018-2019

Hôpital Dupuytren
2018

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...

10.1186/s12964-019-0391-x article EN cc-by Cell Communication and Signaling 2019-08-05

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...

10.4049/jimmunol.1801420 article EN The Journal of Immunology 2019-08-21

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...

10.3389/fimmu.2021.641692 article EN cc-by Frontiers in Immunology 2021-05-04

ABSTRACT How cell-extrinsic niche-related and cell-intrinsic cues drive lineage specification of hematopoietic multipotent progenitors (MPPs) in the bone marrow (BM) is partly understood. We show that CXCR4 signaling strength regulates localization fate MPPs. In mice phenocopying BM myeloid skewing patients with WHIM Syndrome (WS), a rare immunodeficiency caused by gain-of-function mutations, enhanced mTOR overactive Oxphos metabolism were associated rewiring lymphoid-primed MPPs (or MPP4)....

10.1101/2023.05.31.542899 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-06-01

Both cell-intrinsic and niche-derived, cell-extrinsic cues drive the specification of hematopoietic multipotent progenitors (MPPs) in bone marrow, which comprise MPP1 cells lineage-restricted MPP2, MPP3, MPP4 subsets. Patients with WHIM syndrome, a rare congenital immunodeficiency caused by mutations that prevent desensitization chemokine receptor CXCR4, have an excess myeloid marrow. Here, we investigated effects increased CXCR4 signaling on localization fate MPPs. Knock-in mice bearing...

10.1126/scisignal.adl5100 article EN Science Signaling 2024-10-29

WHIM (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis) syndrome is an ultra-rare, combined primary immunodeficiency chronic neutropenic disorder characterized by a range of clinical presentations, including peripheral neutropenia, lymphopenia, recurrent infections. most often caused gain-of-function mutations in the gene encoding C-X-C chemokine receptor 4 (CXCR4). As such, inhibition CXCR4 with XOLREMDI

10.3389/fimmu.2024.1468823 article EN cc-by Frontiers in Immunology 2024-11-11

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...

10.1101/794024 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-10-06

Abstract 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 L.CD40 transgenic mouse model is characterized by specific CD40 signaling responsible NF-κB continuous a spleen monoclonal tumor after one year 60% cases. tumors B-cells expressed high levels PD-L1. This expression was dependent on either NF-κB, JAK1/JAK2 or BTK pathways since ex vivo treatment inhibitory molecules PHA-408, ruxolitinib...

10.1101/502922 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-12-21

Background: Escape from immune control must be important in the natural course of B-cell lymphomas, especially for those with activation NF-kB. Aims: To search PD-L1 expression mouse model L.CD40 that could explain tumor B cells escape surveillance. Methods The pre-clinical transgenic is characterized by specific CD40 signaling responsible NF-kB continuous a spleen monoclonal after one year 60% cases. mice were injected anti-PD-L1 antibody. Results: tumors B-cells expressed high levels...

10.1097/01.hs9.0000566716.49804.5b article EN cc-by-nc-nd HemaSphere 2019-06-01
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