@article{RN25b,

title = {Therapeutic use of CCR5 antagonists is supported by strong expression of CCR5 on CD8(+) T cells in progressive multifocal leukoencephalopathy-associated immune reconstitution inflammatory syndrome},

author = {Martin-Blondel, G. and Bauer, J. and Uro-Coste, E. and Biotti, D. and Averseng-Peaureaux, D. and Fabre, N. and Dumas, H. and Bonneville, F. and Lassmann, H. and Marchou, B. and Liblau, R. S. and Brassat, D.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/25589222},

doi = {10.1007/s00401-015-1383-6},

issn = {1432-0533 (Electronic) 

0001-6322 (Linking)},

year  = {2015},

date = {2015-01-01},

journal = {Acta Neuropathol},

volume = {129},

number = {3},

pages = {463-5},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{spinner_substrates_2015,

title = {Substrates of the ASB2α E3 ubiquitin ligase in dendritic cells},

author = {Spinner, Camille A. and Uttenweiler-Joseph, Sandrine and Metais, Arnaud and Stella, Alexandre and Burlet-Schiltz, Odile and Moog-Lutz, Christel and Lamsoul, Isabelle and Lutz, Pierre G.},

url = {http://www.nature.com/articles/srep16269},

doi = {10.1038/srep16269},

issn = {2045-2322},

year  = {2015},

date = {2015-01-01},

urldate = {2020-09-30},

journal = {Scientific Reports},

volume = {5},

number = {1},

pages = {16269},

abstract = {Conventional dendritic cells (cDCs) comprise distinct populations with specialized immune functions that are mediators of innate and adaptive immune responses. Transcriptomic and proteomic approaches have been used so far to identify transcripts and proteins that are differentially expressed in these subsets to understand the respective functions of cDCs subsets. Here, we showed that the Cullin 5-RING E3 ubiquitin ligase (E3) ASB2α, by driving degradation of filamin A (FLNa) and filamin B (FLNb), is responsible for the difference in FLNa and FLNb abundance in the different spleen cDC subsets. Importantly, the ability of these cDC subsets to migrate correlates with the level of FLNa. Furthermore, our results strongly point to CD4 positive and double negative cDCs as distinct populations. Finally, we develop quantitative global proteomic approaches to identify ASB2α substrates in DCs using ASB2 conditional knockout mice. As component of the ubiquitin-proteasome system (UPS) are amenable to pharmacological manipulation, these approaches aimed to the identification of E3 substrates in physiological relevant settings could potentially lead to novel targets for therapeutic strategies.},

note = {Number: 1 

Publisher: Nature Publishing Group},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{mina_identification_2015,

title = {Identification of Scedosporium boydii catalase A1 gene, a reactive oxygen species detoxification factor highly expressed in response to oxidative stress and phagocytic cells},

author = {Mina, Sara and Staerck, Cindy and d'Almeida, Sènan M. and Marot, Agnès and Delneste, Yves and Calenda, Alphonse and Tabiasco, Julie and Bouchara, Jean-Philippe and Fleury, Maxime J. J.},

doi = {10.1016/j.funbio.2015.09.007},

issn = {1878-6146},

year  = {2015},

date = {2015-01-01},

journal = {Fungal Biology},

volume = {119},

number = {12},

pages = {1322--1333},

abstract = {Scedosporium boydii is an opportunistic filamentous fungus which may be responsible for a large variety of infections in both immunocompetent and immunocompromised individuals. This fungus belongs to the Scedosporium apiospermum species complex which usually ranks second among the filamentous fungi colonizing the airways of patients with cystic fibrosis (CF). Species of the S. apiospermum complex are able to chronically colonize the CF airways suggesting pathogenic mechanisms allowing persistence and growth of these fungi in the respiratory tract. Few putative virulence factors have been purified and characterized so far in the S. apiospermum complex including a cytosolic Cu,Zn-superoxide dismutase (SOD) and a monofunctional catalase (catalase A1). Upon microbial infection, host phagocytes release reactive oxygen species (ROS), such as hydrogen peroxide, as part of the antimicrobial response. Catalases are known to protect pathogens against ROS by degradation of the hydrogen peroxide. Here, we identified the S. boydii catalase A1 gene (CATA1) and investigated its expression in response to the environmental conditions encountered in the CF airways and to the oxidative stress. Results showed that S. boydii CATA1 gene expression is not affected by hypoxia, hypercapnia or pH changes. In contrast, CATA1 gene was overexpressed in response to a chemically induced oxidative stress with a relative gene expression 37-fold higher in the presence of 250 μM H(2)O(2), 20-fold higher with 250 μM menadione and 5-fold higher with 2 mM paraquat. Moreover, S. boydii CATA1 gene expression progressively increased upon exposure to activated THP-1-derived macrophages, reaching a maximum after 12 h (26 fold). Activated HL60-derived neutrophils and activated human peripheral blood neutrophils more rapidly induced S. boydii CATA1 gene overexpression, a maximum gene expression level being reached at 75 min (17 fold) and 60 min (15 fold), respectively. In contrast expression of the gene encoding the Cu,Zn-SOD (SODC gene) was not affected by H(2)O(2), menadione, paraquat or in co-culture with phagocytic cells. These results suggest that S. boydii CATA1 gene is highly stimulated by the oxidative burst response whereas SODC gene is constitutively expressed.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN20b,

title = {Deletion of AU-rich elements within the Bcl2 3'UTR reduces protein expression and B cell survival in vivo},

author = {Diaz-Munoz, M. D. and Bell, S. E. and Turner, M.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/25680182},

doi = {10.1371/journal.pone.0116899},

issn = {1932-6203 (Electronic) 

1932-6203 (Linking)},

year  = {2015},

date = {2015-01-01},

journal = {PLoS One},

volume = {10},

number = {2},

pages = {e0116899},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN19b,

title = {The RNA-binding protein HuR is essential for the B cell antibody response},

author = {Diaz-Munoz, M. D. and Bell, S. E. and Fairfax, K. and Monzon-Casanova, E. and Cunningham, A. F. and Gonzalez-Porta, M. and Andrews, S. R. and Bunik, V. I. and Zarnack, K. and Curk, T. and Heggermont, W. A. and Heymans, S. and Gibson, G. E. and Kontoyiannis, D. L. and Ule, J. and Turner, M.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/25706746},

doi = {10.1038/ni.3115},

issn = {1529-2916 (Electronic) 

1529-2908 (Linking)},

year  = {2015},

date = {2015-01-01},

journal = {Nat Immunol},

volume = {16},

number = {4},

pages = {415-25},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Szelechowski2014,

title = {A viral peptide that targets mitochondria protects against neuronal degeneration in models of Parkinson’s disease},

author = {Marion Szelechowski and Alexandre Bétourné and Yann Monnet and Cécile A. Ferré and Anne Thouard and Charlotte Foret and Jean-Michel Peyrin and Stéphane Hunot and Daniel Gonzalez-Dunia},

doi = {10.1038/ncomms6181},

issn = {2041-1723},

year  = {2014},

date = {2014-12-23},

urldate = {2014-12-23},

journal = {Nat Commun},

volume = {5},

number = {1},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Pendaries2014,

title = {Knockdown of filaggrin in a three-dimensional reconstructed human epidermis impairs keratinocyte differentiation.},

author = {Pendaries, Valérie and Malaisse, Jeremy and Pellerin, Laurence and Le Lamer, Marina and Nachat, Rachida and Kezic, Sanja and Schmitt, Anne-Marie and Paul, Carle and Poumay, Yves and Serre, Guy and Simon, Michel},

doi = {10.1038/jid.2014.259},

issn = {1523-1747 (Electronic)},

year  = {2014},

date = {2014-12-01},

journal = {The Journal of investigative dermatology},

volume = {134},

number = {12},

pages = {2938--2946},

abstract = {Atopic dermatitis is a chronic inflammatory skin disorder characterized by defects in the epidermal barrier and keratinocyte differentiation. The expression of filaggrin, a protein thought to have a major role in the function of the epidermis, is downregulated. However, the impact of this deficiency on keratinocytes is not really known. This was investigated using lentivirus-mediated small-hairpin RNA interference in a three-dimensional reconstructed human epidermis (RHE) model, in the absence of other cell types than keratinocytes. Similar to what is known for atopic skin, the experimental filaggrin downregulation resulted in hypogranulosis, a disturbed corneocyte intracellular matrix, reduced amounts of natural moisturizing factor components, increased permeability and UV-B sensitivity of the RHE, and impaired keratinocyte differentiation at the messenger RNA and protein levels. In particular, the amounts of two filaggrin-related proteins and one protease involved in the degradation of filaggrin, bleomycin hydrolase, were lower. In addition, caspase-14 activation was reduced. These results demonstrate the importance of filaggrin for the stratum corneum properties/functions. They indicate that filaggrin downregulation in the epidermis of atopic patients, either acquired or innate, may be directly responsible for some of the disease-related alterations in the epidermal differentiation program and epidermal barrier function.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Pellerin2014,

title = {Bleomycin hydrolase downregulation in lesional skin of adult atopic dermatitis patients is independent of FLG gene mutations.},

author = {Pellerin, Laurence and Paul, Carle and Schmitt, Anne-Marie and Serre, Guy and Simon, Michel},

doi = {10.1016/j.jaci.2014.07.056},

issn = {1097-6825 (Electronic)},

year  = {2014},

date = {2014-12-01},

journal = {The Journal of allergy and clinical immunology},

volume = {134},

number = {6},

pages = {1459--1461.e7},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Bergboer2014,

title = {Analysis of protein-protein interaction between late cornified envelope proteins and corneodesmosin.},

author = {Bergboer, Judith G M and Dulak, Maria G and van Vlijmen-Willems, Ivonne M J J and Jonca, Nathalie and van Wijk, Erwin and Hendriks, Wiljan J A J and Zeeuwen, Patrick L J M and Schalkwijk, Joost},

doi = {10.1111/exd.12524},

issn = {1600-0625 (Electronic)},

year  = {2014},

date = {2014-10-01},

booktitle = {Experimental dermatology},

journal = {The journal of investigative dermatology},

volume = {23},

number = {10},

pages = {769--771},

abstract = {Deletion of two members of the late cornified envelope (LCE) family, LCE3B and LCE3C (LCE3C_LCE3B-del), has been identified as risk factor for psoriasis with a possible role in skin barrier function. Moreover, genetic interaction between LCE3C_LCE3B-del and HLA-C*06, located in the psoriasis susceptibility regions 4 and 1 (PSORS4 and 1), has been reported in several populations. Because of high linkage disequilibrium between the PSORS1 genes HLA-C*06 and corneodesmosin (CDSN), both genes are potentially involved in psoriasis. As corneodesmosin and LCE proteins are both constituents of the stratum corneum, we investigated potential direct protein-protein interactions between six LCE proteins and two corneodesmosin sequence variants. Partial colocalization of LCE2 and CDSN was observed in normal and psoriasis skin using immunofluorescence microscopy. Co-expression of eCFP-LCE and mRFP-CDSN proteins in COS-1 cells and human adult keratinocytes, and GST pull-down results did not provide evidence for direct interactions between LCE proteins and CDSN variants.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Fredonnet2014,

title = {Topographical and nano-mechanical characterization of native corneocytes using atomic force microscopy.},

author = {Fredonnet, Julie and Gasc, Géraldine and Serre, Guy and Séverac, Childérick and Simon, Michel},

doi = {10.1016/j.jdermsci.2014.04.009},

issn = {1873-569X (Electronic)},

year  = {2014},

date = {2014-07-01},

booktitle = {Journal of dermatological science},

journal = {Journal of dermatological science},

volume = {75},

number = {1},

pages = {63--65},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Leclerc2014,

title = {Mice deficient for the epidermal dermokine $beta$ and $gamma$ isoforms display transient cornification defects.},

author = {Leclerc, Emilie A and Huchenq, Anne and Kezic, Sanja and Serre, Guy and Jonca, Nathalie},

doi = {10.1242/jcs.144808},

issn = {1477-9137 (Electronic)},

year  = {2014},

date = {2014-07-01},

journal = {Journal of cell science},

volume = {127},

number = {Pt 13},

pages = {2862--2872},

abstract = {Expression of the human dermokine gene (DMKN) leads to the production of four dermokine isoform families. The secreted $alpha$, $beta$ and $gamma$ isoforms have an epidermis-restricted expression pattern, with Dmkn $beta$ and $gamma$ being specifically expressed by the granular keratinocytes. The $delta$ isoforms are intracellular and ubiquitous. Here, we performed an in-depth characterization of Dmkn expression in mouse skin and found an expression pattern that was less complex than in humans. In particular, mRNA coding for the $delta$ family were absent. Homozygous mice null for the Dmkn $beta$ and $gamma$ isoforms had no obvious phenotype but only a temporary scaly skin during the first week of life. The pups null for the Dmkn $beta$ and $gamma$ isoforms had smaller keratohyalin granules and their cornified envelopes were more sensitive to mechanical stress. At the molecular level, amounts of profilaggrin and filaggrin monomers were reduced whereas amino acid components of the natural moisturizing factor were increased. In addition, the electrophoretic mobility of involucrin was modified, suggesting post-translational modifications. Finally, the mice null for the Dmkn $beta$ and $gamma$ isoforms strongly overexpressed Dmkn $alpha$. These data are evocative of compensatory mechanisms relevant to the temporary phenotype. Overall, we improved the knowledge of Dmkn expression in mouse and highlighted a role for Dmkn $beta$ and $gamma$ in cornification.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{homedan_acute_2014,

title = {Acute intermittent porphyria causes hepatic mitochondrial energetic failure in a mouse model},

author = {Homedan, Chadi and Laafi, Jihane and Schmitt, Caroline and Gueguen, Naïg and Lefebvre, Thibaud and Karim, Zoubida and Desquiret-Dumas, Valérie and Wetterwald, Céline and Deybach, Jean-Charles and Gouya, Laurent and Puy, Hervé and Reynier, Pascal and Malthièry, Yves},

doi = {10.1016/j.biocel.2014.03.032},

issn = {1878-5875},

year  = {2014},

date = {2014-06-01},

journal = {The International Journal of Biochemistry & Cell Biology},

volume = {51},

pages = {93--101},

abstract = {Acute intermittent porphyria (AIP), an inherited hepatic disorder, is due to a defect of hydroxymethylbilane synthase (HMBS), an enzyme involved in heme biosynthesis. AIP is characterized by recurrent, life-threatening attacks at least partly due to the increased hepatic production of 5-aminolaevulinic acid (ALA). Both the mitochondrial enzyme, ALA synthase (ALAS) 1, involved in the first step of heme biosynthesis, which is closely linked to mitochondrial bioenergetic pathways, and the promise of an ALAS1 siRNA hepatic therapy in humans, led us to investigate hepatic energetic metabolism in Hmbs KO mice treated with phenobarbital. The mitochondrial respiratory chain (RC) and the tricarboxylic acid (TCA) cycle were explored in the Hmbs(-/-) mouse model. RC and TCA cycle were significantly affected in comparison to controls in mice treated with phenobarbital with decreased activities of RC complexes I (-52%, (**)ptextless0.01), II (-50%, (**)ptextless0.01) and III (-55%, (*)ptextless0.05), and decreased activity of α-ketoglutarate dehydrogenase (-64%, (*)ptextless0.05), citrate synthase (-48%, (**)ptextless0.01) and succinate dehydrogenase (-53%, (*)ptextless0.05). Complex II-driven succinate respiration was also significantly affected. Most of these metabolic alterations were at least partially restored after the phenobarbital arrest and heme arginate administration. These results suggest a cataplerosis of the TCA cycle induced by phenobarbital, caused by the massive withdrawal of succinyl-CoA by ALAS induction, such that the TCA cycle is unable to supply the reduced cofactors to the RC. This profound and reversible impact of AIP on mitochondrial energetic metabolism offers new insights into the beneficial effect of heme, glucose and ALAS1 siRNA treatments by limiting the cataplerosis of TCA cycle.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Hayez2014,

title = {High TMEM45A expression is correlated to epidermal keratinization.},

author = {Hayez, Aurélie and Malaisse, Jérémy and Roegiers, Edith and Reynier, Marie and Renard, Chantal and Haftek, Marek and Geenen, Vincent and Serre, Guy and Simon, Michel and de Rouvroit, Catherine Lambert and Michiels, Carine and Poumay, Yves},

doi = {10.1111/exd.12403},

issn = {1600-0625 (Electronic)},

year  = {2014},

date = {2014-05-01},

journal = {Experimental dermatology},

volume = {23},

number = {5},

pages = {339--344},

abstract = {TMEM45A (DERP7, DNAPTP4 or FLJ10134) gene, belonging to the TMEM family encoding predicted transmembrane proteins, is highly expressed in epidermal keratinocytes. To investigate the potential involvement of TMEM45A during the differentiation and keratinization processes, its expression has been characterized in normal human keratinocytes and the protein subcellular localization has been studied in this cell type, both in vitro and in vivo. TMEM45A expression is upregulated with differentiation, either induced by cultured keratinocyte confluence or enhanced Ca(2+) concentration in medium. In vivo, TMEM45A mRNA and protein are mostly found in the granular layer of the epidermis. TMEM45A expression is linked to keratinization, as accumulation of the protein is detected in native and reconstructed epidermis as well as in thymic Hassal bodies, but not in non-keratinized stratified epithelia. At the subcellular level, co-detection with ER and Golgi markers reveals that TM protein 45A is associated with the Golgi apparatus and more specifically with the trans-Golgi/trans-Golgi network in vitro and in granular layer in vivo. The protein is neither related to lysosomes nor transported within corneodesmosin-containing lamellar bodies. These data demonstrate a strong correlation between TMEM45A expression and epidermal keratinization, indicating the relevance of this gene in this process.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{oustric_antisense_2014,

title = {Antisense oligonucleotide-based therapy in human erythropoietic protoporphyria},

author = {Oustric, Vincent and Manceau, Hana and Ducamp, Sarah and Soaid, Rima and Karim, Zoubida and Schmitt, Caroline and Mirmiran, Arienne and Peoc'h, Katell and Grandchamp, Bernard and Beaumont, Carole and Lyoumi, Said and Moreau-Gaudry, François and Guyonnet-Dupérat, Véronique and de Verneuil, Hubert and Marie, Joëlle and Puy, Herve and Deybach, Jean-Charles and Gouya, Laurent},

doi = {10.1016/j.ajhg.2014.02.010},

issn = {1537-6605},

year  = {2014},

date = {2014-04-01},

journal = {American Journal of Human Genetics},

volume = {94},

number = {4},

pages = {611--617},

abstract = {In 90% of people with erythropoietic protoporphyria (EPP), the disease results from the inheritance of a common hypomorphic FECH allele, encoding ferrochelatase, in trans to a private deleterious FECH mutation. The activity of the resulting FECH enzyme falls below the critical threshold of 35%, leading to the accumulation of free protoporphyrin IX (PPIX) in bone marrow erythroblasts and in red cells. The mechanism of low expression involves a biallelic polymorphism (c.315-48TtextgreaterC) localized in intron 3. The 315-48C allele increases usage of the 3' cryptic splice site between exons 3 and 4, resulting in the transcription of an unstable mRNA with a premature stop codon, reducing the abundance of wild-type FECH mRNA, and finally reducing FECH activity. Through a candidate-sequence approach and an antisense-oligonucleotide-tiling method, we identified a sequence that, when targeted by an antisense oligonucleotide (ASO-V1), prevented usage of the cryptic splice site. In lymphoblastoid cell lines derived from symptomatic EPP subjects, transfection of ASO-V1 reduced the usage of the cryptic splice site and efficiently redirected the splicing of intron 3 toward the physiological acceptor site, thereby increasing the amount of functional FECH mRNA. Moreover, the administration of ASO-V1 into developing human erythroblasts from an overtly EPP subject markedly increased the production of WT FECH mRNA and reduced the accumulation of PPIX to a level similar to that measured in asymptomatic EPP subjects. Thus, EPP is a paradigmatic Mendelian disease in which the in vivo correction of a common single splicing defect would improve the condition of most affected individuals.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN9b,

title = {Ribavirin for chronic hepatitis E virus infection in transplant recipients},

author = {Kamar, N. and Izopet, J. and Tripon, S. and Bismuth, M. and Hillaire, S. and Dumortier, J. and Radenne, S. and Coilly, A. and Garrigue, V. and D'Alteroche, L. and Buchler, M. and Couzi, L. and Lebray, P. and Dharancy, S. and Minello, A. and Hourmant, M. and Roque-Afonso, A. M. and Abravanel, F. and Pol, S. and Rostaing, L. and Mallet, V.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/24645943},

doi = {10.1056/NEJMoa1215246},

issn = {1533-4406 (Electronic) 

0028-4793 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {N Engl J Med},

volume = {370},

number = {12},

pages = {1111-20},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN28,

title = {Impairment of adipose tissue in Prader-Willi syndrome rescued by growth hormone treatment},

author = {Cadoudal, T. and Buleon, M. and Sengenes, C. and Diene, G. and Desneulin, F. and Molinas, C. and Eddiry, S. and Conte-Auriol, F. and Daviaud, D. and Martin, P. G. and Bouloumie, A. and Salles, J. P. and Tauber, M. and Valet, P.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/24406482},

doi = {10.1038/ijo.2014.3},

issn = {1476-5497 (Electronic) 

0307-0565 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {Int J Obes (Lond)},

volume = {38},

number = {9},

pages = {1234-40},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN30,

title = {Modulation of pro-inflammatory activation of monocytes and dendritic cells by aza-bis-phosphonate dendrimer as an experimental therapeutic agent},

author = {Degboé Y and Fruchon S and Baron M and Nigon D and Turrin CO and Caminade AM and Poupot R and Cantagrel A and JL, Davignon},

year  = {2014},

date = {2014-01-01},

journal = {Arthritis Research and Therapy},

volume = {16},

number = {R98},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN5b,

title = {Monocyte-derived dendritic cells promote T follicular helper cell differentiation},

author = {Chakarov, S. and Fazilleau, N.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/24737871},

doi = {10.1002/emmm.201403841},

issn = {1757-4684 (Electronic) 

1757-4676 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {EMBO Mol Med},

volume = {6},

pages = {590-603},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN6b,

title = {A prospective observational post-marketing study of natalizumab-treated multiple sclerosis patients: clinical, radiological and biological features and adverse events. The BIONAT cohort},

author = {Outteryck, O. and Ongagna, J. C. and Brochet, B. and Rumbach, L. and Lebrun-Frenay, C. and Debouverie, M. and Zephir, H. and Ouallet, J. C. and Berger, E. and Cohen, M. and Pittion, S. and Laplaud, D. and Wiertlewski, S. and Cabre, P. and Pelletier, J. and Rico, A. and Defer, G. and Derache, N. and Camu, W. and Thouvenot, E. and Moreau, T. and Fromont, A. and Tourbah, A. and Labauge, P. and Castelnovo, G. and Clavelou, P. and Casez, O. and Hautecoeur, P. and Papeix, C. and Lubetzki, C. and Fontaine, B. and Couturier, N. and Bohossian, N. and Clanet, M. and Vermersch, P. and de Seze, J. and Brassat, D. and Network, Bionat and Cfsep},

url = {http://www.ncbi.nlm.nih.gov/pubmed/23895407},

doi = {10.1111/ene.12204},

issn = {1468-1331 (Electronic) 

1351-5101 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {Eur J Neurol},

volume = {21},

number = {1},

pages = {40-8},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN5,

title = {X-Chromosome complement and estrogen receptor signaling independently contribute to the enhanced TLR7-mediated IFN-alpha production of plasmacytoid dendritic cells from women},

author = {Laffont, S. and Rouquie, N. and Azar, P. and Seillet, C. and Plumas, J. and Aspord, C. and Guery, J. C.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/25339659 

http://www.jimmunol.org/content/193/11/5444.full.pdf},

doi = {10.4049/jimmunol.1303400},

issn = {1550-6606 (Electronic) 

0022-1767 (Linking)},

year  = {2014},

date = {2014-01-01},

journal = {J Immunol},

volume = {193},

number = {11},

pages = {5444-52},

keywords = {},

pubstate = {published},

tppubtype = {article}

}