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Centre d'immunologie de Marseille-Luminy

(Redirected from Centre d’Immunologie de Marseille-Luminy)
"CIML" redirects here. For other uses, see CIML (disambiguation).

The Centre d'Immunologie de Marseille-Luminy (CIML) was founded in 1976 and has been described by AERES, an independent evaluation agency, as "without doubt one of the best immunology centers of excellence in Europe".[1] The CIML addresses all areas of contemporary immunology; it is located in Marseille in the South of France.[2]

CIML entrance
The CIML.

Function

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The institute has 17 research teams, with 250 staff including 185 scientists, students, and post-docs from 24 countries. It offers Masters and PhD programs.[3]

The CIML has 90 academic collaborations and 21 industrial partners in France, Europe, and worldwide, and has formed several spin-offs, including: Innate Pharma, Ipsogen (Quiagen), and Immunotech (Beckman-Coulter).[citation needed]

The institute has published over 400 scientific publications in the last 5 years, including 145 in journals with an impact factor ≥ 10.[4]

It is located on a science campus that is home to more than 1,500 researchers and 10,000 students, and 15 biotech companies.[5]

Directors

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  • François Kourilsky, 1976–1977
  • Michel Fougerau 1978–1980
  • François Kourilsky, 1981–1984
  • Pierre Golstein, 1985-1988[6]
  • Bertrand Jordan, 1989–1990
  • Michel Pierres, 1991–1994
  • Bernard Malissen, 1995-2005[7]
  • Jean Pierre Gorvel 2006-2008[8]
  • Eric Vivier, 2008 - 2017[9]

Advances in immunology made through discoveries at the CIML

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Early work at CIML was centered on T cells. The study of their antigen receptors lead to the discovery of chromosomal inversion during the formation of the T cell receptor (TCR).[10] Researchers at the CIML also published the first nucleotide sequence of a gene encoding a human major histocompatibility complex (MHC) gene [11] and described how the TCR recognizes its MHC ligand.[12] The functions of these T cells were also investigated, leading in particular to the identification of Granzyme A and GZMB (then called CTLA-1 and CTLA-3)[13] and the demonstration of their playing a role in the perforin-granzyme-based mechanism of T-cell-mediated cytotoxicity, and to the discovery of the second, Fas ligand/Fas receptor based pathway of cytotoxicity.[14][15] Other biologically important regulatory molecules identified at the CIML include interleukins such as interleukin-17 (as CTLA-8)[16] and cell surface molecules, such as CTLA-4[17] regulating T cells. Subsequently, research at the CIML expanded to other cells of the immune system, including B cells, dendritic cells and natural killer cells, as well as other models systems, such as C. elegans.[18] CIML researchers identified the immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing KARAP/DAP12[19] that is important for NK cell function and characterized the key function of the killer activated receptor NKp46.[20] Other recent advances include the discovery of early precursors of B-cell follicular lymphoma in apparently healthy individuals,[21] and of dendritic cell aggresome-like induced structures (DALIS) in dendritic cells,[22] thought to play an important role in regulating antigen presentation, as well as the discovery of MafB/M-CSF circuits in hematopoietic stem cell commitment, and macrophages.[23][24]

Funding

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The CIML is mainly supported by direct and indirect funding from INSERM, the CNRS, and Aix-Marseille University, covering for example the salaries of more than 125 permanent staff members. Other major funders include the European Research Council, European Union, the Agence Nationale de la Recherche, Association pour la Recherche sur le Cancer, Fondation Recherche Medicale, Human Frontier Science Program, Institut National du Cancer, La Ligue Nationale Contre le Cancer, as well as CIML's industrial partners.[citation needed]

Education and training

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The CIML's Master's and PhD program is integrated into the educational framework of Aix-Marseille University. Participation in the CIML program requires enrollment in the Master's-PhD program at the Ecole Doctorale des Sciences de la Vie. A unique part of the program is a student exchange scheme with Harvard Medical School.[citation needed]

Clinical activities

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In immunology, more than in any other discipline, physiology is often revealed by pathology. Therefore, the institute is involved in many studies with clinical objectives. A wide range of malignancies are studied at the CIML such as leukemias and hematopoietic cancers, lymphomas and primary immune deficiencies, or brucellosis and juvenile arthritis. Treatments are also a major concern of the institute, such as studies on the prevention, monitoring, and treatment of hematologic malignancies and on the impact of therapies on the immune system. Finally, theoretical work which may provide key solutions to medicine are performed at the CIML on inflammatory mechanisms associated with the development of inflammatory bowel.[citation needed]

References

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  1. ^ "AERES 2011 report on the CIML" (PDF). www.aeres-evaluation.fr. Archived from the original (PDF) on 2015-05-18. Retrieved 2012-04-01.
  2. ^ "CIML | Welcome to the Centre d'Immunologie de Marseille-Luminy". Ciml.univ-mrs.fr. Archived from the original on 2012-04-03. Retrieved 2012-04-01.
  3. ^ "The CIML Master PhD Immunology Program | CIML". Ciml.univ-mrs.fr. Archived from the original on 2015-06-01. Retrieved 2012-04-01.
  4. ^ "Web of Knowledge - IP & Science - Thomson Reuters". Archived from the original on 2020-01-23. Retrieved 2012-04-01.
  5. ^ "Accueil | Faculté des Sciences de Luminy". Sciences.univmed.fr. Archived from the original on 2012-04-15. Retrieved 2012-04-01.
  6. ^ "Pierre GOLSTEIN, MD, PhD" (PDF). ciml.univ-mrs.fr. June 20, 2011. Archived (PDF) from the original on 6 July 2022. Retrieved 3 July 2024.
  7. ^ "Bernard MALLISEN, PhD Marie MALLISEN, PhD" (PDF). ciml.univ-mrs.fr. June 20, 2011. Archived (PDF) from the original on 6 July 2024. Retrieved 3 July 2024.
  8. ^ "Jean-Pierre GORVEL, PhD" (PDF). ciml.univ-mrs.fr. June 20, 2011. Archived (PDF) from the original on 1 June 2023. Retrieved 3 July 2024.
  9. ^ "Eric VIVIER" (PDF). ciml.univ-mrs.fr. June 20, 2011. Archived (PDF) from the original on 7 July 2022. Retrieved 3 July 2024.
  10. ^ Malissen, M; McCoy, C; Blanc, D; Trucy, J; Devaux, C; Schmitt-Verhulst, AM; Fitch, F; Hood, L; Malissen, B (1986). "Direct evidence for chromosomal inversion during T-cell receptor β-gene rearrangements". Nature. 319 (6048): 28–33. Bibcode:1986Natur.319...28M. doi:10.1038/319028a0. PMID 3484541. S2CID 4285220.
  11. ^ Malissen, M; Malissen, B; Jordan, BR (1982). "Exon/intron organization and complete nucleotide sequence of an HLA gene". PNAS. 79 (3): 893–7. Bibcode:1982PNAS...79..893M. doi:10.1073/pnas.79.3.893. PMC 345859. PMID 6461010.
  12. ^ Reiser, JB; Darnault, C; Guimezanes, A; Grégoire, C; Mosser, T; Schmitt-Verhulst, AM; Fontecilla-Camps, JC; Malissen, B; et al. (2000). "Crystal structure of a T cell receptor bound to an allogeneic MHC molecule". Nature Immunology. 1 (4): 291–7. doi:10.1038/79728. PMID 11017099. S2CID 428937.
  13. ^ Brunet, JF; Dosseto, M; Denizot, F; Mattei, MG; Clark, WR; Haqqi, TM; Ferrier, P; Nabholz, M; et al. (1986). "The inducible cytotoxic T-lymphocyte-associated gene transcript CTLA-1 sequence and gene localization to mouse chromosome 14". Nature. 322 (6076): 268–71. Bibcode:1986Natur.322..268B. doi:10.1038/322268a0. PMID 3090449. S2CID 4317126.
  14. ^ Rouvier, E; Luciani, MF; Golstein, P (1993). "Fas involvement in Ca(2+)-independent T cell-mediated cytotoxicity". Journal of Experimental Medicine. 177 (1): 195–200. doi:10.1084/jem.177.1.195. PMC 2190860. PMID 7678113.
  15. ^ Kägi, D; Vignaux, F; Ledermann, B; Burki, K; Depraetere, V; Nagata, S; Hengartner, H; Golstein, P (1994). "Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity". Science. 265 (5171): 528–30. Bibcode:1994Sci...265..528K. doi:10.1126/science.7518614. PMID 7518614.
  16. ^ Rouvier, E; Luciani, MF; Mattéi, MG; Denizot, F; Golstein, P (1993). "CTLA-8, cloned from an activated T cell, bearing AU-rich messenger RNA instability sequences, and homologous to a herpesvirus saimiri gene". Journal of Immunology. 150 (12): 5445–56. doi:10.4049/jimmunol.150.12.5445. PMID 8390535. S2CID 5802339.
  17. ^ Brunet, JF; Denizot, F; Luciani, MF; Roux-Dosseto, M; Suzan, M; Mattei, MG; Golstein, P (1987). "A new member of the immunoglobulin superfamily--CTLA-4". Nature. 328 (6127): 267–70. Bibcode:1987Natur.328..267B. doi:10.1038/328267a0. PMID 3496540. S2CID 4316396.
  18. ^ Mallo, GV; Kurz, CL; Couillault, C; Pujol, N; Granjeaud, S; Kohara, Y; Ewbank, JJ (2002). "Inducible antibacterial defense system in C. Elegans". Current Biology. 12 (14): 1209–14. doi:10.1016/S0960-9822(02)00928-4. PMID 12176330.
  19. ^ Tomasello, E; Olcese, L; Vély, F; Geourgeon, C; Bléry, M; Moqrich, A; Gautheret, D; Djabali, M; et al. (1998). "Gene structure, expression pattern, and biological activity of mouse killer cell activating receptor-associated protein (KARAP)/DAP-12". Journal of Biological Chemistry. 273 (51): 34115–9. doi:10.1074/jbc.273.51.34115. PMID 9852069.
  20. ^ Narni-Mancinelli, E; Jaeger, BN; Bernat, C; Fenis, A; Kung, S; De Gassart, A; Mahmood, S; Gut, M; et al. (2012). "Tuning of Natural Killer Cell Reactivity by NKp46 and Helios Calibrates T Cell Responses". Science. 335 (6066): 344–8. Bibcode:2012Sci...335..344N. doi:10.1126/science.1215621. PMID 22267813. S2CID 12914956.
  21. ^ Roulland, S; Navarro, JM; Grenot, P; Milili, M; Agopian, J; Montpellier, B; Gauduchon, P; Lebailly, P; et al. (2006). "Follicular lymphoma-like B cells in healthy individuals: A novel intermediate step in early lymphomagenesis". Journal of Experimental Medicine. 203 (11): 2425–31. doi:10.1084/jem.20061292. PMC 2118129. PMID 17043145.
  22. ^ Lelouard, H; Gatti, E; Cappello, F; Gresser, O; Camosseto, V; Pierre, P (2002). "Transient aggregation of ubiquitinated proteins during dendritic cell maturation". Nature. 417 (6885): 177–82. Bibcode:2002Natur.417..177L. doi:10.1038/417177a. PMID 12000969. S2CID 4399462.
  23. ^ Sarrazin, S; Mossadegh-Keller, N; Fukao, T; Aziz, A; Mourcin, F; Vanhille, L; Kelly Modis, L; Kastner, P; et al. (2009). "MafB restricts M-CSF-dependent myeloid commitment divisions of hematopoietic stem cells". Cell. 138 (2): 300–13. doi:10.1016/j.cell.2009.04.057. PMID 19632180.
  24. ^ Aziz, A; Soucie, E; Sarrazin, S; Sieweke, MH (2009). "MafB/c-Maf deficiency enables self-renewal of differentiated functional macrophages". Science. 326 (5954): 867–71. Bibcode:2009Sci...326..867A. doi:10.1126/science.1176056. PMID 19892988. S2CID 6446747.
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