@article{RN163,

title = {Hematopoietic chimerism and transplantation tolerance: a role for regulatory T cells},

author = {Pasquet, Lise and Joffre, Olivier and Santolaria, Thibault and van Meerwijk, Joost},

url = {http://www.frontiersin.org/Journal/Abstract.aspx?s=1180&name=immunological_tolerance&ART_DOI=10.3389/fimmu.2011.00080},

doi = {10.3389/fimmu.2011.00080},

issn = {1664-3224},

year  = {2011},

date = {2011-01-01},

journal = {Frontiers in Immunology},

volume = {2},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN162,

title = {AIRE-deficient CD8+CD28low regulatory T lymphocytes fail to control experimental colitis},

author = {Pomie, C. and Vicente, R. and Vuddamalay, Y. and Ardesjö Lundgren, B. and van der Hoek, M. and Enault, G. and Kagan, J. and Fazilleau, N and Scott, H. S. and Romagnoli, P. and van Meerwijk, J.P.M.},

year  = {2011},

date = {2011-01-01},

journal = {Proceedings of the National Academy of Sciences of the U.S.A.},

volume = {108},

number = {30},

pages = {12437-12442},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN14b,

title = {The p.Arg63Trp polymorphism controls Vav1 functions and Foxp3 regulatory T cell development},

author = {Colacios, C. and Casemayou, A. and Dejean, A. S. and Gaits-Iacovoni, F. and Pedros, C. and Bernard, I. and Lagrange, D. and Deckert, M. and Lamouroux, L. and Jagodic, M. and Olsson, T. and Liblau, R. S. and Fournie, G. J. and Saoudi, A.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/21948080},

doi = {10.1084/jem.20102191},

issn = {1540-9538 (Electronic) 

0022-1007 (Linking)},

year  = {2011},

date = {2011-01-01},

journal = {J Exp Med},

volume = {208},

number = {11},

pages = {2183-91},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN8b,

title = {Tyrosine kinase 2 variant influences T lymphocyte polarization and multiple sclerosis susceptibility},

author = {Couturier, N. and Bucciarelli, F. and Nurtdinov, R. N. and Debouverie, M. and Lebrun-Frenay, C. and Defer, G. and Moreau, T. and Confavreux, C. and Vukusic, S. and Cournu-Rebeix, I. and Goertsches, R. H. and Zettl, U. K. and Comabella, M. and Montalban, X. and Rieckmann, P. and Weber, F. and Muller-Myhsok, B. and Edan, G. and Fontaine, B. and Mars, L. T. and Saoudi, A. and Oksenberg, J. R. and Clanet, M. and Liblau, R. S. and Brassat, D.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/21354972},

doi = {10.1093/brain/awr010},

issn = {1460-2156 (Electronic) 

0006-8950 (Linking)},

year  = {2011},

date = {2011-01-01},

journal = {Brain},

volume = {134},

number = {Pt 3},

pages = {693-703},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN18b,

title = {Highly specialized role of Forkhead box O transcription factors in the immune system},

author = {Dejean, A. S. and Hedrick, S. M. and Kerdiles, Y. M.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/20673126},

doi = {10.1089/ars.2010.3414},

issn = {1557-7716 (Electronic) 

1523-0864 (Linking)},

year  = {2011},

date = {2011-01-01},

journal = {Antioxid Redox Signal},

volume = {14},

number = {4},

pages = {663-74},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN7b,

title = {Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis},

author = {International Multiple Sclerosis Genetics, Consortium and Wellcome Trust Case Control, Consortium and Sawcer, S. and Hellenthal, G. and Pirinen, M. and Spencer, C. C. and Patsopoulos, N. A. and Moutsianas, L. and Dilthey, A. and Su, Z. and Freeman, C. and Hunt, S. E. and Edkins, S. and Gray, E. and Booth, D. R. and Potter, S. C. and Goris, A. and Band, G. and Oturai, A. B. and Strange, A. and Saarela, J. and Bellenguez, C. and Fontaine, B. and Gillman, M. and Hemmer, B. and Gwilliam, R. and Zipp, F. and Jayakumar, A. and Martin, R. and Leslie, S. and Hawkins, S. and Giannoulatou, E. and D'Alfonso, S. and Blackburn, H. and Martinelli Boneschi, F. and Liddle, J. and Harbo, H. F. and Perez, M. L. and Spurkland, A. and Waller, M. J. and Mycko, M. P. and Ricketts, M. and Comabella, M. and Hammond, N. and Kockum, I. and McCann, O. T. and Ban, M. and Whittaker, P. and Kemppinen, A. and Weston, P. and Hawkins, C. and Widaa, S. and Zajicek, J. and Dronov, S. and Robertson, N. and Bumpstead, S. J. and Barcellos, L. F. and Ravindrarajah, R. and Abraham, R. and Alfredsson, L. and Ardlie, K. and Aubin, C. and Baker, A. and Baker, K. and Baranzini, S. E. and Bergamaschi, L. and Bergamaschi, R. and Bernstein, A. and Berthele, A. and Boggild, M. and Bradfield, J. P. and Brassat, D. and Broadley, S. A. and Buck, D. and Butzkueven, H. and Capra, R. and Carroll, W. M. and Cavalla, P. and Celius, E. G. and Cepok, S. and Chiavacci, R. and Clerget-Darpoux, F. and Clysters, K. and Comi, G. and Cossburn, M. and Cournu-Rebeix, I. and Cox, M. B. and Cozen, W. and Cree, B. A. and Cross, A. H. and Cusi, D. and Daly, M. J. and Davis, E. and de Bakker, P. I. and Debouverie, M. and D'Hooghe M, B. and Dixon, K. and Dobosi, R. and Dubois, B. and Ellinghaus, D. and others},

url = {http://www.ncbi.nlm.nih.gov/pubmed/21833088},

doi = {10.1038/nature10251},

issn = {1476-4687 (Electronic) 

0028-0836 (Linking)},

year  = {2011},

date = {2011-01-01},

journal = {Nature},

volume = {476},

number = {7359},

pages = {214-9},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Sec22b regulates phagosomal maturation and antigen crosspresentation by dendritic cells},

author = {Cebrian, I. and Visentin, G. and Blanchard, N. and Jouve, M. and Bobard, A. and Moita, C. and Enninga, J. and Moita, L. F. and Amigorena, S. and Savina, A.},

year  = {2011},

date = {2011-01-01},

journal = {Cell},

volume = {147},

number = {6},

pages = {1355-68},

abstract = {Antigen (Ag) crosspresentation by dendritic cells (DCs) involves the presentation of internalized Ags on MHC class I molecules to initiate CD8+ T cell-mediated immunity in response to certain pathogens and tumor cells. Here, we identify the SNARE Sec22b as a specific regulator of Ag crosspresentation. Sec22b localizes to the ER-Golgi intermediate compartment (ERGIC) and pairs to the plasma membrane SNARE syntaxin 4, which is present in phagosomes (Phgs). Depletion of Sec22b inhibits the recruitment of ER-resident proteins to Phgs and to the vacuole containing the Toxoplasma gondii parasite. In Sec22b-deficient DCs, crosspresentation is compromised after Ag phagocytosis or endocytosis and after invasion by T. gondii. Sec22b silencing inhibited Ag export to the cytosol and increased phagosomal degradation by accelerating lysosomal recruitment. Our findings provide insight into an intracellular traffic pathway required for crosspresentation and show that Sec22b-dependent recruitment of ER proteins to Phgs critically influences phagosomal functions in DCs.},

note = {Cebrian, Ignacio 

Visentin, Geraldine 

Blanchard, Nicolas 

Jouve, Mabel 

Bobard, Alexandre 

Moita, Catarina 

Enninga, Jost 

Moita, Luis F 

Amigorena, Sebastian 

Savina, Ariel 

Cell. 2011 Dec 9;147(6):1355-68.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Sec22b regulates phagosomal maturation and antigen crosspresentation by dendritic cells},

author = {Cebrian, I. and Visentin, G. and Blanchard, N. and Jouve, M. and Bobard, A. and Moita, C. and Enninga, J. and Moita, L. F. and Amigorena, S. and Savina, A.},

year  = {2011},

date = {2011-01-01},

journal = {Cell},

volume = {147},

number = {6},

pages = {1355-68},

abstract = {Antigen (Ag) crosspresentation by dendritic cells (DCs) involves the presentation of internalized Ags on MHC class I molecules to initiate CD8+ T cell-mediated immunity in response to certain pathogens and tumor cells. Here, we identify the SNARE Sec22b as a specific regulator of Ag crosspresentation. Sec22b localizes to the ER-Golgi intermediate compartment (ERGIC) and pairs to the plasma membrane SNARE syntaxin 4, which is present in phagosomes (Phgs). Depletion of Sec22b inhibits the recruitment of ER-resident proteins to Phgs and to the vacuole containing the Toxoplasma gondii parasite. In Sec22b-deficient DCs, crosspresentation is compromised after Ag phagocytosis or endocytosis and after invasion by T. gondii. Sec22b silencing inhibited Ag export to the cytosol and increased phagosomal degradation by accelerating lysosomal recruitment. Our findings provide insight into an intracellular traffic pathway required for crosspresentation and show that Sec22b-dependent recruitment of ER proteins to Phgs critically influences phagosomal functions in DCs.},

note = {Dec 9;147(6):1355-68.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Coudane2011,

title = {Deimination and expression of peptidylarginine deiminases during cutaneous wound healing in mice.},

author = {Coudane, Fanny and Méchin, Marie-Claire and Huchenq, Anne and Henry, Julie and Nachat, Rachida and Ishigami, Akihito and Adoue, Véronique and Sebbag, Mireille and Serre, Guy and Simon, Michel},

doi = {10.1684/ejd.2011.1394},

issn = {1167-1122 (Print)},

year  = {2011},

date = {2011-01-01},

journal = {European journal of dermatology : EJD},

volume = {21},

number = {3},

pages = {376--384},

abstract = {Deimination, the conversion of protein-bound arginines into citrullines, is a post-translational modification catalyzed by a peptidylarginine deiminase (Pad). In the epidermis, three Pads are expressed, namely Pad1, 2 and 3, and the major deiminated protein is filaggrin. Deimination of fibrin has been observed in various pathological inflammatory conditions. Here, we analyzed the expression of Pads and citrullination of proteins during cutaneous wound healing, i.e. in a physiological inflammatory condition. Full-thickness punches were performed on adult mouse back skin, and wound recovery was analyzed over 10 days by immunohistology and western blotting. Pad1 was immunodetected in all the neo-epidermis. Pad3, normally expressed in the stratum granulosum, was not detected in the hyperproliferative tongue of the neo-epidermis, but was shown to be co-localized with (pro)filaggrin in a large number of keratinocyte layers in its differentiating part. Deiminated proteins were detected in the stratum corneum of the neo-epidermis in the late phase of re-epithelialization, and in the clot and the clot-derived scab. In the clot where we only detected Pad4, one of the deiminated proteins was shown to be fibrin. Deimination of the clot proteins, and more generally wound healing and keratinocyte differentiation, seemed to be Pad2-independent, as shown using Padi2(-/-) mice.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Paul2011,

title = {Prevalence and risk factors for xerosis in the elderly: a cross-sectional epidemiological study in primary care.},

author = {Paul, C and Maumus-Robert, S and Mazereeuw-Hautier, J and Guyen, C N and Saudez, X and Schmitt, A M},

doi = {10.1159/000334631},

issn = {1421-9832 (Electronic)},

year  = {2011},

date = {2011-01-01},

journal = {Dermatology (Basel, Switzerland)},

volume = {223},

number = {3},

pages = {260--265},

abstract = {BACKGROUND: Limited information is available concerning the prevalence and risk factors of xerosis in the elderly. OBJECTIVE: To establish the prevalence of xerosis and associated factors in elderly patients. METHODS: A national, multicenter, observational, cross-sectional study in patients aged 65 or older was performed. The data collected by general practitioners were demographics and medical history, including history of atopic disease. Xerosis was evaluated using the Overall Dry Skin score. RESULTS: 756 patients were included. The prevalence of xerosis was 55.6%. Xerosis was significantly associated with older age (OR: 1.48, 95% CI: 1.16-1.89), female sex (OR: 1.80, 95 CI%: 1.29-2.53), treatments that can potentially cause xerosis (OR: 2.21, 95 CI%: 1.54-3.17), itching during sweating (OR: 7.11, 95% CI: 3.90-12.95), a history of dry skin (OR: 2.89, 95% CI: 1.65-5.08) and a history of atopic dermatitis (OR: 3.60, 95% CI: 1.99-6.52). CONCLUSION: Xerosis is highly prevalent in the elderly. A history of atopy, especially atopic dermatitis, is associated with an increased risk of xerosis in the elderly.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{millot_erythropoietin_2010,

title = {Erythropoietin stimulates spleen BMP4-dependent stress erythropoiesis and partially corrects anemia in a mouse model of generalized inflammation},

author = {Millot, Sarah and Andrieu, Valérie and Letteron, Philippe and Lyoumi, Saïd and Hurtado-Nedelec, Margarita and Karim, Zoubida and Thibaudeau, Olivier and Bennada, Samira and Charrier, Jean-Luc and Lasocki, Sigismond and Beaumont, Carole},

doi = {10.1182/blood-2010-04-281840},

issn = {1528-0020},

year  = {2010},

date = {2010-12-01},

journal = {Blood},

volume = {116},

number = {26},

pages = {6072--6081},

abstract = {Mouse bone marrow erythropoiesis is homeostatic, whereas after acute anemia, bone morphogenetic protein 4 (BMP4)-dependent stress erythropoiesis develops in the spleen. The aim of this work was to compare spleen stress erythropoiesis and bone marrow erythropoiesis in a mouse model of zymosan-induced generalized inflammation, which induces long-lasting anemia and to evaluate the ability of erythropoietin (Epo) injections to correct anemia in this setting. The effects of zymosan and/or Epo injections on erythroid precursor maturation and apoptosis, serum interferon-γ levels, hematologic parameters, and spleen BMP4 expression were analyzed, as well as the effect of zymosan on red blood cell half-life. We found that bone marrow erythropoiesis is suppressed by inflammation and does not respond to Epo administration, despite repression of erythroblast apoptosis. On the contrary, a robust erythropoietic response takes place in the spleen after Epo injections in both control and zymosan-induced generalized inflammation mice. This specific response implies Epo-mediated induction of BMP4 expression by F4/80(+) spleen macrophages, proliferation of stress burst-forming units-erythroid, and increased number of spleen erythroblasts. It allows only partial recovery of anemia, probably because of peripheral destruction of mature red cells. It is not clear whether similar BMP4-dependent stress erythropoiesis can occur in human bone marrow after Epo injections.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Schmid2010,

title = {Protein kinase C-dependent phosphorylation of Borna disease virus P protein is required for efficient viral spread},

author = {Sonja Schmid and Philippe Metz and Christine M. A. Prat and Daniel Gonzalez-Dunia and Martin Schwemmle},

doi = {10.1007/s00705-010-0645-9},

issn = {1432-8798},

year  = {2010},

date = {2010-05-00},

urldate = {2010-05-00},

journal = {Arch Virol},

volume = {155},

number = {5},

pages = {789--793},

publisher = {Springer Science and Business Media LLC},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN14b,

title = {Maintenance of cytomegalovirus-specific CD4pos T-cell response in rheumatoid arthritis patients receiving anti-tumor necrosis factor treatments},

author = {Davignon, J. L. and Boyer, J. F. and Jamard, B. and Nigon, D. and Constantin, A. and Cantagrel, A.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/20633267},

doi = {10.1186/ar3083},

issn = {1478-6362 (Electronic) 

1478-6354 (Linking)},

year  = {2010},

date = {2010-01-01},

journal = {Arthritis Res Ther},

volume = {12},

number = {4},

pages = {R142},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN156,

title = {Thymic selection and lineage commitment of CD4+Foxp3+ regulatory T lymphocytes},

author = {Romagnoli, P. and van Meerwijk, J. P. M.},

year  = {2010},

date = {2010-01-01},

journal = {Prog Mol Biol Transl Sci.},

volume = {92},

pages = {251-77},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{szutkowska_zeta-crystallin_2009,

title = {Zeta-crystallin mediates the acid pH-induced increase of BSC1 cotransporter mRNA stability},

author = {Szutkowska, Marta and Vernimmen, Catherine and Debaix, Huguette and Devuyst, Olivier and Friedlander, Gérard and Karim, Zoubida},

doi = {10.1038/ki.2009.265},

issn = {1523-1755},

year  = {2009},

date = {2009-10-01},

journal = {Kidney International},

volume = {76},

number = {7},

pages = {730--738},

abstract = {The Na+/K+/2Cl- cotransporter (BSC1/NKCC2) is the major transporter mediating sodium chloride and ammonium absorption in the medullary thick ascending limb. A loss-of-function mutation of BSC1 is responsible for Bartter's syndrome. We previously showed both in vivo and in vitro that acidosis increases the expression and activity of BSC1 and that acid pH enhances the stability of BSC1 mRNA by mechanisms involving its 3'-untranslated region (UTR). zeta-Crystallin is a pH response factor that protects the mitochondrial glutaminase mRNA by a specific interaction with AU-rich motifs. Here we identified the molecular determinant(s) within the 3'-UTR that are responsible for BSC1-mRNA expression and assessed the involvement of zeta-crystallin in this regulation. Deleting three out of six conserved AU-rich motifs drastically reduced the expression of BSC1-mRNA with maximal effect for motif 3 at position 870 of the 3'UTR. This motif was responsible for pH and zeta-crystallin-induced stability of BSC1 mRNA. The abundance of zeta-crystallin was increased by acid pH and its overexpression increased the stability of BSC1 mRNA, but its RNA silencing inhibited acid pH-induced BSC1 expression. Therefore the 3'UTR of BSC1-mRNA is a target for zeta-crystallin. The induction of zeta-crystallin by an acid pH plays an important role in preventing BSC1 mRNA decay, thus increasing its expression and activity.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Prat2009,

title = {Mutation of the Protein Kinase C Site in Borna Disease Virus Phosphoprotein Abrogates Viral Interference with Neuronal Signaling and Restores Normal Synaptic Activity},

author = {Christine M. A. Prat and Sonja Schmid and Fanny Farrugia and Nicolas Cenac and Gwendal Le Masson and Martin Schwemmle and Daniel Gonzalez-Dunia},

editor = {Raul Andino},

doi = {10.1371/journal.ppat.1000425},

issn = {1553-7374},

year  = {2009},

date = {2009-05-08},

urldate = {2009-05-08},

journal = {PLoS Pathog},

volume = {5},

number = {5},

publisher = {Public Library of Science (PLoS)},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN19,

title = {Transcription factor Foxo3 controls the magnitude of T cell immune responses by modulating the function of dendritic cells},

author = {Dejean, A. S. and Beisner, D. R. and Ch'en, I. L. and Kerdiles, Y. M. and Babour, A. and Arden, K. C. and Castrillon, D. H. and DePinho, R. A. and Hedrick, S. M.},

url = {http://www.ncbi.nlm.nih.gov/pubmed/19363483},

doi = {10.1038/ni.1729},

issn = {1529-2916 (Electronic) 

1529-2908 (Linking)},

year  = {2009},

date = {2009-01-01},

journal = {Nat Immunol},

volume = {10},

number = {5},

pages = {504-13},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{karim_nherf1_2008,

title = {NHERF1 mutations and responsiveness of renal parathyroid hormone},

author = {Karim, Zoubida and Gérard, Bénédicte and Bakouh, Naziha and Alili, Rohia and Leroy, Christine and Beck, Laurent and Silve, Caroline and Planelles, Gabrielle and Urena-Torres, Pablo and Grandchamp, Bernard and Friedlander, Gérard and Prié, Dominique},

doi = {10.1056/NEJMoa0802836},

issn = {1533-4406},

year  = {2008},

date = {2008-09-01},

journal = {The New England Journal of Medicine},

volume = {359},

number = {11},

pages = {1128--1135},

abstract = {Impaired renal phosphate reabsorption, as measured by dividing the tubular maximal reabsorption of phosphate by the glomerular filtration rate (TmP/GFR), increases the risks of nephrolithiasis and bone demineralization. Data from animal models suggest that sodium-hydrogen exchanger regulatory factor 1 (NHERF1) controls renal phosphate transport. We sequenced the NHERF1 gene in 158 patients, 94 of whom had either nephrolithiasis or bone demineralization. We identified three distinct mutations in seven patients with a low TmP/GFR value. No patients with normal TmP/GFR values had mutations. The mutants expressed in cultured renal cells increased the generation of cyclic AMP (cAMP) by parathyroid hormone (PTH) and inhibited phosphate transport. These NHERF1 mutations suggest a previously unrecognized cause of renal phosphate loss in humans.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Immunodominant, protective response to the parasite Toxoplasma gondii requires antigen processing in the endoplasmic reticulum},

author = {Blanchard, N. and Gonzalez, F. and Schaeffer, M. and Joncker, N. T. and Cheng, T. and Shastri, A. J. and Robey, E. A. and Shastri, N.},

year  = {2008},

date = {2008-01-01},

journal = {Nat Immunol},

volume = {9},

number = {8},

pages = {937-44},

abstract = {The parasite Toxoplasma gondii replicates in a specialized intracellular vacuole and causes disease in many species. Protection from toxoplasmosis is mediated by CD8(+) T cells, but the T. gondii antigens and host genes required for eliciting protective immunity are poorly defined. Here we identified GRA6, a polymorphic protein secreted in the parasitophorous vacuole, as the source of the immunodominant and protective decapeptide HF10 presented by the H-2L(d) major histocompatibility complex class I molecule. Presentation of the HF10-H-2L(d) ligand required proteolysis by ERAAP, the endoplasmic reticulum aminopeptidase associated with antigen processing. Consequently, expansion of protective CD8(+) T cell populations was impaired in T. gondii-infected ERAAP-deficient mice, which were more susceptible to toxoplasmosis. Thus, endoplasmic reticulum proteolysis is critical for eliciting protective immunity to a vacuolar parasite.},

note = {NLM 

In-Process 

Journal Article 

Research Support, N.I.H., Extramural 

Research Support, Non-U.S. Gov't DEP - 20080629},

keywords = {},

pubstate = {published},

tppubtype = {article}

}