Talk:Centre d'immunologie de Marseille-Luminy

Contested deletion
This page is not unambiguously promotional, because:

(i) The information is presented in as neutral a fashion possible.

(ii) It was modeled on a number of other wikipedia entries for equivalent internationally known non-for profit research institutes. To cite one example: European_Bioinformatics_Institute

(iii) A part of the original motivation was that the page Yang_Huanming refers to the CIML, but there was no explanation of what the CIML is.

Having said that, any necessary editing to bring it more into line with Wikipedia guidelines are welcome.

CIML wiki (talk) 21:15, 31 January 2012 (UTC)Jonathan Ewbank (for CIML wiki)

Status and Advice
I noticed that the institute is so very notable, that it was worth the rewriting. Make certain none of the text is copied from elsewhere. Listing the departments in a table is  unusual, but I see no rule against it. The second table, on medical projects, should be converted to prose, with the project titles as footnotes. Please see if you can make articles on the people claimed as notable alumni: see WP:PROF for the guideline, and articles on other scientists for the format. (What in effect is basically wanted in this field for each is at least a few papers with over a hundred citations each; preferably h=20, or greater. ) Watch out about those photos: they must be licensed formally according to WP:DCM following every detail; what is present in the credit lines is not sufficient.  DGG ( talk ) 03:56, 1 February 2012 (UTC)

Response of original contributors
Many thanks for these helpful and constructive remarks. We've tried to edit as you suggested. For the time being, we've removed the Alumuni section, which included:

Jean-François Brunet, Michel Delaage, Christian Devaux, Michel Fougereau, Christo Goridis, Yang Huanming, François Kourilsky, Eric Meffre, Genevieve Rougon, Quentin Sattentau,

as for the moment, only Yang Huanming, founder of Beijing Genomics Institute has an entry. If and when pages are made for at least a couple of the others, we'd hope to see the section return.

Thanks again.

PS. Editing from "CIML wiki" has been disabled by Smartse. We understand the reason and won't use that account again.

Descotes (talk) 09:55, 1 February 2012 (UTC) Jonathan Ewbank and Nicolas Descotes


 * You imply that your account is being used by more than one person, this is strictly against Wikipedia policy.Theroadislong (talk) 12:08, 1 February 2012 (UTC)

Descotes is a single-person account (see User_talk:Theroadislong). With regards the "A major contributor to this article appears to have a close connection with its subject" tag, I put the page together to start the ball rolling. As DGG said, the CIML is a world-class institute. I'd be really pleased if anyone could edit out anything that looks biased. Again, I modeled it on a number of other uncontested wikipedia entries for scientific institutes. Descotes (talk) 13:51, 1 February 2012 (UTC)Nicolas

Response regarding notability and references
I include below some information that may contribute to establish the notability of the CIML.

In March 2011, the independent evaluation body, the AERES (http://www.aeres-evaluation.com/) published a 4-year review of the CIML. They wrote, “The CIML is without doubt one of the best immunology centers of excellence in Europe”.

http://www.aeres-evaluation.fr/content/download/16630/263864/file/B2012-EV-0131843H-S2UR120001648-RD.pdf

The perceived notability could also be reinforced if a text such as the following were to be included.

Discoveries made at the CIML
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) [1]. Researchers at the CIML also published the first nucleotide sequence of a gene encoding a human major histocompatibility complex (MHC) gene [2] and described how the TCR recognizes its MHC ligand [3]. The functions of these T cells were also investigated, leading in particular to the identification of Granzymes A and GZMB (then called CTLA-1 and CTLA-3) [4] 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 [5,6]. Other biologically important regulatory molecules identified at the CIML include interleukins such as Interleukin-17 (as CTLA-8) [7] and cell surface molecules, such as CTLA-4 [8] regulating T cells. Subsequently, research at the CIML expanded to other cells of the immune system, including B cells, dendritic cells and Natural Killer (NK) cells, as well as other models systems, such as ‘’C. elegans’’ [9]. CIML researchers identified the Immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing KARAP/DAP12 [10] that is important for NK cell function and characterized the key function of the Killer activating receptor NKp46 [11]. Other recent advances include the discovery of early precursors of B-cell follicular lymphoma in apparently healthy individuals [12], and of dendritic cell aggresome-like induced structures (DALIS) in dendritic cells [13], 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 [14, 15].

1	Malissen, M. et al. Direct evidence for chromosomal inversion during T-cell receptor beta-gene rearrangements. Nature 319, 28-33, doi:10.1038/319028a0 (1986).

2	Malissen, M., Malissen, B. & Jordan, B. R. Exon/intron organization and complete nucleotide sequence of an HLA gene. Proceedings of the National Academy of Sciences of the United States of America 79, 893-897 (1982).

3	Reiser, J. B. et al. Crystal structure of a T cell receptor bound to an allogeneic MHC molecule. Nat Immunol 1, 291-297, doi:10.1038/79728 (2000).

4	Brunet, J.-F. et al. The inducible cytotoxic-T-lymphocyte-associated gene transcript CTLA-1 sequence and gene localization to mouse chromosome 14. Nature 322, 268-271 (1986).

5	Rouvier, E., Luciani, M.-F. & Golstein, P. Fas involvement in Ca++-independent T cell-mediated cytotoxicity. Journal of Experimental Medicine 177, 195-200 (1993).

6	Kägi, D. et al. Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity. Science (New York, N.Y 265, 528-530 (1994).

7	Rouvier, E., Luciani, M.-F., Mattéi, M.-G., Denizot, F. & Golstein, P. 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, 5445-5456 (1993).

8	Brunet, J.-F. et al. A new member of the immunoglobulin superfamily - CTLA-4. Nature 328, 267-270 (1987).

9	Mallo, G. V. et al. Inducible antibacterial defense system in C. elegans. Current biology : CB 12, 1209-1214 (2002).

10	Tomasello, E. et al. Gene structure, expression pattern, and biological activity of mouse killer cell activating receptor-associated protein (KARAP)/DAP-12. The Journal of biological chemistry 273, 34115-34119 (1998).

11	Narni-Mancinelli, E. et al. Tuning of natural killer cell reactivity by NKp46 and Helios calibrates T cell responses. Science (New York, N.Y) 335, 344-348, doi:10.1126/science.1215621 (2012).

12	Roulland, S. et al. Follicular lymphoma-like B cells in healthy individuals: a novel intermediate step in early lymphomagenesis. The Journal of experimental medicine 203, 2425-2431, doi:10.1084/jem.20061292 (2006).

13	Lelouard, H. et al. Transient aggregation of ubiquitinated proteins during dendritic cell maturation. Nature 417, 177-182, doi:10.1038/417177a (2002).

14	Sarrazin, S. et al. MafB restricts M-CSF-dependent myeloid commitment divisions of hematopoietic stem cells. Cell 138, 300-313, doi:S0092-8674(09)00518-2 [pii] 10.1016/j.cell.2009.04.057 (2009).

15	MafB/c-Maf deficiency enables self-renewal of differentiated functional macrophages. Aziz, A., et al. Science (New York, N.Y) 326, 867-871, (2009).

Descotes (talk) 20:31, 19 February 2012 (UTC)Nicolas