Centre d'Immunology Marseille-Luminy (CIML), Inserm
Host : P. Martineau (IRCM)
We longitudinally tracked the B-cell repertoires of 10 individuals after SARS-CoV-2 infection and repeated vaccinations. We reconstructed in vitro the naive sequences of a curated selection of 10,000 clonal lineages and measured their affinity for the spike protein binding domain of SARS-CoV-2. Our findings reveal that while the overall properties of the repertoire, including diversity, expansion, and V-gene usage, remained stable and similar to healthy individuals, the 'binder' lineages, whose naive sequence is capable of antigen binding, expanded more and had higher mutation rates. Their evolutionary patterns also differed markedly from non-binders. Among the binders, the high-affinity binder lineages showed the most activity and diversified more across the time points. We also demonstrate that lineages with identical naive sequences in different individuals evolve in similar ways. This comprehensive dataset of antibody-spike interactions in a real-world setting provides insights into detecting reacting clones within a repertoire and helps us understand how the functional diversity of the naive repertoire shapes the adaptive immune response to vaccination.
School of International Business, China Pharmaceutical University (CPU), China
This presentation offers a comparative overview of drug reimbursement policies for anticancer therapies across Asia and France, with a particular focus on oncology. Drawing on large-scale health insurance databases and electronic health record (EHR) systems, our team examines how reimbursement criteria and pharmaceutical benefits are shaped by real-world evidence, including safety profiles and treatment efficacy observed in patient cohorts. We aim to highlight key similarities and differences across health systems, and to discuss implications for policy and clinical practice
host: Prof E. DESHAYES (ICM)
Singapore-Sichuan Frontier Medical Center, West China Hospital,
Institute of Thoracic Oncology, Chengdu, China
host: A. David (IRCM)
Equipe "Cancer, Metabolism & Environment"
Inserm U1065/ Université Côte d'Azur (Nice)
Centre Méditerranéen de Médecine Moléculaire (C3M)
host: Eric JULIEN (IRCM)
Professor Lung Inflammation and Repair
Institute for Lung Health - Justus Liebig University
German Center for Lung Research, GIESSEN (Germany)
host : A. MARAVER (IRCM)
Chronic lung disease such as IPF or COPD develops over extended periods of time and are
characterized by failure in mechanisms of repair (1,2). Both pathologies are considered age-related
diseases exhibiting most of the hallmarks of aging including stem cell exhaustion and altered
intercellular communication (3). In the last years, novel epithelial progenitor cells have been identified
and demonstrated to contribute to lung repair. In fact, distinct subpopulations of alveolar type (AT) 2
cells have been shown to have higher regenerative capacity (4-8). Recent findings shed light to the
mechanisms of regeneration of the alveolar epithelium (8-11); however, a better understanding of the
coordinated processes of tissue repair from different stem cell pools after injury is crucial to restore
the delicate lung architecture. Our research focuses on the study of the interplay between these
epithelial progenitor populations and neighboring cell types of their microenvironment in the
development of lung disease.
It is now generally accepted that epithelial cell loss or dysfunction drives the development of lung
fibrosis (12-15). We have identified an additional function for AT2 cells that in addition to serve as
adult stem cells of the alveolar epithelium can play a profibrotic role directly activating adjacent
fibroblast. This communication is mediated by the Notch pathway and their blockade seems to
attenuate the fibrotic phenotype, revealing a potential therapy for IPF, a fatal disease with no cure, a
median survival of 3-5 years post-diagnosis and whose incidence in increasing in the last years (1).
Thus, our findings support the notion that the pathophysiology of pulmonary fibrosis relies in part, on
the Notch-regulated interaction between aberrant cellular populations of the fibrotic lung and that
unravelling this complex microenvironment is critical to find efficient treatments for IPF.
References
1. Schneider JL, et al. The aging lung: physiology, disease and immunity. Cell. 2021 Apr
15;184(8):1990-2019. doi: 10.1016/j.cell.2021.03.005.
2. Han S, et al. Alveolar epithelial regeneration in the aging lung. .J Clin Invest. 2023 Oct
16;133(20):e170504. doi: 10.1172/JCI170504
3. Lopez-Otin C. et al. Hallmarks of aging: An expanding universe. Cell 2023, Jan 19;186(2):243-278.
doi: 10.1016/j.cell.2022.11.001
4. Zacharias WJ. et al, Nature 2018 Mar 8;555(7695):251-255. doi: 10.1038/nature25786.
5. Nabhan AN. et al., Science 2018 Mar 9;359(6380):1118-1123. doi: 10.1126/science.aam6603
6. Chen et al., Am J Physiol Lung Cell Mol Physiol. 2017 Jul 1;313(1):L41-L51. doi:
10.1152/ajplung.00564.2016.
7. Ahmadvand N. et al., Eur Respir J. 2021 Nov 4;58(5):2004168. doi: 10.1183/13993003.04168-
2020.
8. Choi J. et al., Cell Stem Cell 2020 Sep 3;27(3):366-382.e7. doi: 10.1016/j.stem.2020.06.020.
9. Kobayashi Y. et al, Nat Cell Biol 2020 Aug;22(8):934-946. doi: 10.1038/s41556-020-0542-8.
10. Strunz M. et al., Nat Comm 2020. Jul 16;11(1):3559. doi: 10.1038/s41467-020-17358-3.
11. Jiang P. et al., Am J Respir Crit Care Med. 2020 Jun 1;201(11):1443-1447. doi:
10.1164/rccm.201909-1726LE.
12. Sakai, N. & Tager, A. M. Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary
fibrosis. Biochim. Biophys. Acta - Mol. Basis Dis. 1832, 911–921 (2013).
13. Barkauskas, C. E. & Noble, P. W. Cellular Mechanisms of Tissue Fibrosis. 7. New insights into the
cellular mechanisms of pulmonary fibrosis. AJP Cell Physiol. 306, C987–C996 (2014).
14. Xie T. et al. Abnormal respiratory progenitors in fibrotic lung injury. Stem Cell Res Ther.;13(1):64
(2022).
15. Konkimalla A, et al. Lung Regeneration: Cells, Models, and Mechanisms. Cold Spring Harb
Perspect Biol.; a040873 (2021).
Institut Pasteur (Paris)
hosts: Alexandre David & Laurent Le Cam (IRCM)
ROUEN University, INSERM U982
host : A. Maraver (IRCM)
Cancer research UK (CRUK) Manchester Institute
host : L. Le CAM (IRCM)
Department of Oncology, Faculty of Medicine and Dentistry, University of Alberta
host : Alexandre Djiane (IRCM)
Physiological Sciences Department, Faculty of Science, Stellenbosch University, South Africa.
Resia Pretorius is a Distinguished Professor at Stellenbosch University (South Africa), Honorary Professor at the University of Liverpool, and founding director of Biocode Technologies. Her research focuses on how inflammation disrupts coagulation and immune function, leading to microclots, platelet activation, and endothelial pathology across diseases including cancer, diabetes, cardiovascular disease and Long COVID. She has published over 330 papers, filed multiple patents on microclot diagnostics, and serves on global health advisory panels including the WHO.
host : Alain R. Thierry (IRCM)
Senior Lecturer,
City St George's, University of London
host : (N. Bonnefoy, IRCM)
selected publications :
Bacevic K*, Noble R*, Soffar A, Ammar OW, Boszonyik B, Prieto S, Vincent C, Hochberg ME, Krasinska L, Fisher D. Spatial competition constrains resistance to targeted cancer therapy. Nature Communications (2017) 8, 1995
Viossat Y, Noble R. A theoretical analysis of tumour containment. Nature Ecology & Evolution (2021)
Patil S, Viossat Y, Noble R. Preventing evolutionary rescue in cancer. bioRxiv (2023)
Université Libre de Bruxelles
host : Laurent Le Cam (IRCM)
Located in the Parc Euromédecine, the Institut de Recherche en Cancérologie de Montpellier (U1194) is located on the Val d'Aurelle Campus (ICM, Institut régional du Cancer Montpellier/ Val d'Aurelle).
U1194 Research Centre supported by Inserm, the University of Montpellier and the Institut du Cancer de Montpellier (ICM)
Institut de Recherche en Cancérologie de