@article{RN47b,

title = {Real-life assessment of the multidimensional nature of dyspnoea in COPD outpatients},

author = {Morelot-Panzini, C. and Gilet, H. and Aguilaniu, B. and Devillier, P. and Didier, A. and Perez, T. and Pignier, C. and Arnould, B. and Similowski, T.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27076585},

doi = {10.1183/13993003.01998-2015},

issn = {1399-3003 (Electronic) 

0903-1936 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {Eur Respir J},

volume = {47},

number = {6},

pages = {1668-79},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN52b,

title = {Bronchoscopic Multimodal Management of Tracheal Neurofibroma},

author = {Rabeau, A. and Mazieres, J. and Hermant, C. and Projetti, F. and Didier, A. and Guibert, N.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/26496086},

doi = {10.1097/LBR.0000000000000220},

issn = {1948-8270 (Electronic) 

1948-8270 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {J Bronchology Interv Pulmonol},

volume = {23},

number = {4},

pages = {340-342},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN53b,

title = {Mast cells in asthma: biomarker and therapeutic target},

author = {Reber, L. L. and Fahy, J. V.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27037311},

doi = {10.1183/13993003.00065-2016},

issn = {1399-3003 (Electronic) 

0903-1936 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {Eur Respir J},

volume = {47},

number = {4},

pages = {1040-2},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN54b,

title = {Neutrophils are not required for resolution of acute gouty arthritis in mice},

author = {Reber, L. L. and Gaudenzio, N. and Starkl, P. and Galli, S. J.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27923029},

doi = {10.1038/nm.4216},

issn = {1546-170X (Electronic) 

1078-8956 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {Nat Med},

volume = {22},

number = {12},

pages = {1382-1384},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN59b,

title = {Development of a drug delivery system for efficient alveolar delivery of a neutralizing monoclonal antibody to treat pulmonary intoxication to ricin},

author = {Respaud, R. and Marchand, D. and Pelat, T. and Tchou-Wong, K. M. and Roy, C. J. and Parent, C. and Cabrera, M. and Guillemain, J. and Mac Loughlin, R. and Levacher, E. and Fontayne, A. and Douziech-Eyrolles, L. and Junqua-Moullet, A. and Guilleminault, L. and Thullier, P. and Guillot-Combe, E. and Vecellio, L. and Heuze-Vourc'h, N.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27173943},

doi = {10.1016/j.jconrel.2016.05.018},

issn = {1873-4995 (Electronic) 

0168-3659 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {J Control Release},

volume = {234},

pages = {21-32},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN64,

title = {A TNFRSF14-FcvarepsilonRI-mast cell pathway contributes to development of multiple features of asthma pathology in mice},

author = {Sibilano, R. and Gaudenzio, N. and DeGorter, M. K. and Reber, L. L. and Hernandez, J. D. and Starkl, P. M. and Zurek, O. W. and Tsai, M. and Zahner, S. and Montgomery, S. B. and Roers, A. and Kronenberg, M. and Yu, M. and Galli, S. J.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27982078},

doi = {10.1038/ncomms13696},

issn = {2041-1723 (Electronic) 

2041-1723 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {Nat Commun},

volume = {7},

pages = {13696},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN66b,

title = {IgE antibodies, FcepsilonRIalpha, and IgE-mediated local anaphylaxis can limit snake venom toxicity},

author = {Starkl, P. and Marichal, T. and Gaudenzio, N. and Reber, L. L. and Sibilano, R. and Tsai, M. and Galli, S. J.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/26410782},

doi = {10.1016/j.jaci.2015.08.005},

issn = {1097-6825 (Electronic) 

0091-6749 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {J Allergy Clin Immunol},

volume = {137},

number = {1},

pages = {246-257 e11},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{RN1013,

title = {Interactions between Flow Oscillations and Biochemical Parameters in the Cerebrospinal Fluid},

author = {Puy, V. and Zmudka-Attier, J. and Capel, C. and Bouzerar, R. and Serot, J. M. and Bourgeois, A. M. and Ausseil, J. and Baledent, O.},

url = {https://www.ncbi.nlm.nih.gov/pubmed/27445797},

doi = {10.3389/fnagi.2016.00154},

issn = {1663-4365 (Print) 

1663-4365 (Linking)},

year  = {2016},

date = {2016-01-01},

journal = {Front Aging Neurosci},

volume = {8},

pages = {154},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{Hamdi2016,

title = {Association of breast cancer risk with genetic variants showing differential allelic expression: Identification of a novel breast cancer susceptibility locus at 4q21},

author = {Hamdi, Y and Soucy, P and Adoue, V and Michailidou, K and Canisius, S and Lemaçon, A and Droit, A and Andrulis, I L and Anton-Culver, H and Arndt, V and Baynes, C and Blomqvist, C and Bogdanova, N V and Bojesen, S E and Bolla, M K and Bonanni, B and Borresen-Dale, AL and Brand, J S and Brauch, H and Brenner, H and Broeks, A and Burwinkel, B and Chang-Claude, J and Couch, F J and Cox, A and Cross, S S and Czene, K and Darabi, H and Dennis, J and Devilee, Pr and Dörk, T and Dos-Santos-Silva, I and Eriksson, M and Fasching, P A and Figueroa, J and Flyger, H and Garcia-Closas, M and Giles, G G and Goldberg, M S and Gonzalez-Neira, A and Grenaker-Alnaes, G and Guénel, P and Haeberle, L and Haiman, C A and Hamann, U and Hallberg, E and Hooning, M J and Hopper, J L and Jakubowska, A and Jones, M and Kabisch, M and Kataja, V and Lambrechts, D and Le Marchand, Land Lindblom, A and Lubinski, Jand Mannermaa, A and Maranian, M and Margolin, S and Marme, F and Milne, R L and Neuhausen, S L and Nevanlinna, H and Neven, P and Olswold, C and Peto, J and Plaseska-Karanfilska, D and Pylkäs, K and Radice, P and Rudolph, A and Sawyer, E J and Schmidt, M K and Shu, X O and Southey, M C and Swerdlow, A and Tollenaar, R A E M and Tomlinson, I and Torres, D and Truong, T and Vachon, C and Van Den Ouweland, A M W and Wang, Q and Winqvist, R and Zheng, W and Benitez, J and Chenevix-Trench, G and Dunning, A M. and Pharoah, P D P and Kristensen, V and Hall, P and Easton, D F and Pastinen, T and Nord, S and Simard, J},

doi = {10.18632/oncotarget.12818},

issn = {19492553},

year  = {2016},

date = {2016-01-01},

journal = {Oncotarget},

abstract = {There are significant inter-individual differences in the levels of gene expression. Through modulation of gene expression, cis-acting variants represent an important source of phenotypic variation. Consequently, cis-regulatory SNPs associated with differential allelic expression are functional candidates for further investigation as disease-causing variants. To investigate whether common variants associated with differential allelic expression were involved in breast cancer susceptibility, a list of genes was established on the basis of their involvement in cancer related pathways and/or mechanisms. Thereafter, using data from a genome-wide map of allelic expression associated SNPs, 313 genetic variants were selected and their association with breast cancer risk was then evaluated in 46,451 breast cancer cases and 42,599 controls of European ancestry ascertained from 41 studies participating in the Breast Cancer Association Consortium. The associations were evaluated with overall breast cancer risk and with estrogen receptor negative and positive disease. One novel breast cancer susceptibility locus on 4q21 (rs11099601) was identified (OR = 1.05},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Rab22a controls MHC-I intracellular trafficking and antigen cross-presentation by dendritic cells},

author = {Cebrian, I. and Croce, C. and Guerrero, N. A. and Blanchard, N. and Mayorga, L. S.},

year  = {2016},

date = {2016-01-01},

journal = {EMBO Rep},

abstract = {Cross-presentation by MHC class I molecules allows the detection of exogenous antigens by CD8+ T lymphocytes. This process is crucial to initiate cytotoxic immune responses against many pathogens (i.e., Toxoplasma gondii) and tumors. To achieve efficient cross-presentation, dendritic cells (DCs) have specialized endocytic pathways; however, the molecular effectors involved are poorly understood. In this work, we identify the small GTPase Rab22a as a key regulator of MHC-I trafficking and antigen cross-presentation by DCs. Our results demonstrate that Rab22a is recruited to DC endosomes and phagosomes, as well as to the vacuole containing T. gondii parasites. The silencing of Rab22a expression did not affect the uptake of exogenous antigens or parasite invasion, but it drastically reduced the intracellular pool and the recycling of MHC-I molecules. The knockdown of Rab22a also hampered the cross-presentation of soluble, particulate and T. gondii-associated antigens, but not the endogenous MHC-I antigen presentation through the classical secretory pathway. Our findings provide compelling evidence that Rab22a plays a central role in the MHC-I endocytic trafficking, which is crucial for efficient cross-presentation by DCs.},

note = {Cebrian, Ignacio 

Croce, Cristina 

Guerrero, Nestor A 

Blanchard, Nicolas 

Mayorga, Luis S 

England 

EMBO Rep. 2016 Oct 10. pii: e201642358.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Continuous Effector CD8(+) T Cell Production in a Controlled Persistent Infection Is Sustained by a Proliferative Intermediate Population},

author = {Chu, H. H. and Chan, S. W. and Gosling, J. P. and Blanchard, N. and Tsitsiklis, A. and Lythe, G. and Shastri, N. and Molina-Paris, C. and Robey, E. A.},

year  = {2016},

date = {2016-01-01},

journal = {Immunity},

volume = {45},

number = {1},

pages = {159-71},

abstract = {Highly functional CD8(+) effector T (Teff) cells can persist in large numbers during controlled persistent infections, as exemplified by rare HIV-infected individuals who control the virus. Here we examined the cellular mechanisms that maintain ongoing T effector responses using a mouse model for persistent Toxoplasma gondii infection. In mice expressing the protective MHC-I molecule, H-2L(d), a dominant T effector response against a single parasite antigen was maintained without a contraction phase, correlating with ongoing presentation of the dominant antigen. Large numbers of short-lived Teff cells were continuously produced via a proliferative, antigen-dependent intermediate (Tint) population with a memory-effector hybrid phenotype. During an acute, resolved infection, decreasing antigen load correlated with a sharp drop in the Tint cell population and subsequent loss of the ongoing effector response. Vaccination approaches aimed at the development of Tint populations might prove effective against pathogens that lead to chronic infection.},

note = {Chu, H Hamlet 

Chan, Shiao-Wei 

Gosling, John Paul 

Blanchard, Nicolas 

Tsitsiklis, Alexandra 

Lythe, Grant 

Shastri, Nilabh 

Molina-Paris, Carmen 

Robey, Ellen A 

Immunity. 2016 Jul 19;45(1):159-71. doi: 10.1016/j.immuni.2016.06.013. Epub 2016 Jul 12.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Erythroferrone contributes to hepcidin repression in a mouse model of malarial anemia},

author = {Latour, C. and Wlodarczyk, M. F. and Jung, G. and Gineste, A. and Blanchard, N. and Ganz, T. and Roth, M. P. and Coppin, H. and Kautz, L.},

year  = {2016},

date = {2016-01-01},

journal = {Haematologica},

abstract = {Malaria, a major global health challenge worldwide, is accompanied by a severe anemia secondary to hemolysis and increased erythrophagocytosis. Iron is an essential functional component of erythrocyte hemoglobin and its availability is controlled by the liver-derived hormone hepcidin. We examined the regulation of hepcidin during malarial infection in mice using the rodent parasite Plasmodium berghei K173 (PbK). Mice infected with PbK develop a severe anemia and die after 18 to 22 days without cerebral malaria. During the early phase of blood-stage infection (day 1 to 5), a strong inflammatory signature was associated with increased production of hepcidin. Between days 7 and 18, while infection progresses, red blood cell count, hemoglobin and hematocrit dramatically decreased. In the late phase of malarial infection, hepcidin production was reduced concomitantly to an increase in the mRNA expression of the hepcidin suppressor erythroferrone (ERFE) in the bone marrow and the spleen. Compared with wild-type mice, Erfe-/- mice failed to adequately suppress hepcidin expression after infection with PbK. Importantly, the sustained production of hepcidin allowed by ERFE ablation was associated with decreased parasitemia, providing further evidence that transient iron restriction could be beneficial in the treatment of malaria.},

note = {Latour, Chloe 

Wlodarczyk, Myriam F 

Jung, Grace 

Gineste, Aurelie 

Blanchard, Nicolas 

Ganz, Tomas 

Roth, Marie-Paule 

Coppin, Helene 

Kautz, Leon 

Haematologica. 2016 Sep 22. pii: haematol.2016.150227.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {A Worldwide Map of Plasmodium falciparum K13-Propeller Polymorphisms},

author = {Menard, D. and Khim, N. and Beghain, J. and Adegnika, A. A. and Shafiul-Alam, M. and Amodu, O. and Rahim-Awab, G. and Barnadas, C. and Berry, A. and Boum, Y. and Bustos, M. D. and Cao, J. and Chen, J. H. and Collet, L. and Cui, L. and Thakur, G. D. and Dieye, A. and Djalle, D. and Dorkenoo, M. A. and Eboumbou-Moukoko, C. E. and Espino, F. E. and Fandeur, T. and Ferreira-da-Cruz, M. F. and Fola, A. A. and Fuehrer, H. P. and Hassan, A. M. and Herrera, S. and Hongvanthong, B. and Houze, S. and Ibrahim, M. L. and Jahirul-Karim, M. and Jiang, L. and Kano, S. and Ali-Khan, W. and Khanthavong, M. and Kremsner, P. G. and Lacerda, M. and Leang, R. and Leelawong, M. and Li, M. and Lin, K. and Mazarati, J. B. and Menard, S. and Morlais, I. and Muhindo-Mavoko, H. and Musset, L. and Na-Bangchang, K. and Nambozi, M. and Niare, K. and Noedl, H. and Ouedraogo, J. B. and Pillai, D. R. and Pradines, B. and Quang-Phuc, B. and Ramharter, M. and Randrianarivelojosia, M. and Sattabongkot, J. and Sheikh-Omar, A. and Silue, K. D. and Sirima, S. B. and Sutherland, C. and Syafruddin, D. and Tahar, R. and Tang, L. H. and Toure, O. A. and Tshibangu-wa-Tshibangu, P. and Vigan-Womas, I. and Warsame, M. and Wini, L. and Zakeri, S. and Kim, S. and Eam, R. and Berne, L. and Khean, C. and Chy, S. and Ken, M. and Loch, K. and Canier, L. and Duru, V. and Legrand, E. and Barale, J. C. and Stokes, B. and Straimer, J. and Witkowski, B. and Fidock, D. A. and Rogier, C. and Ringwald, P. and Ariey, F. and Mercereau-Puijalon, O.},

year  = {2016},

date = {2016-01-01},

journal = {N Engl J Med},

volume = {374},

number = {25},

pages = {2453-64},

abstract = {BACKGROUND: Recent gains in reducing the global burden of malaria are threatened by the emergence of Plasmodium falciparum resistance to artemisinins. The discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domains are the major determinant of resistance has provided opportunities for monitoring such resistance on a global scale. METHODS: We analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic. Most of the samples (84.5%) were obtained from patients who were treated at sentinel sites used for nationwide surveillance of antimalarial resistance. We evaluated the emergence and dissemination of mutations by haplotyping neighboring loci. RESULTS: We identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution. In Asia, 36.5% of the K13 mutations were distributed within two areas--one in Cambodia, Vietnam, and Laos and the other in western Thailand, Myanmar, and China--with no overlap. In Africa, we observed a broad array of rare nonsynonymous mutations that were not associated with delayed parasite clearance. The gene-edited Dd2 transgenic line with the A578S mutation, which expresses the most frequently observed African allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay. CONCLUSIONS: No evidence of artemisinin resistance was found outside Southeast Asia and China, where resistance-associated K13 mutations were confined. The common African A578S allele was not associated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neutral. (Funded by Institut Pasteur Paris and others.).},

note = {Menard, Didier 

Khim, Nimol 

Beghain, Johann 

Adegnika, Ayola A 

Shafiul-Alam, Mohammad 

Amodu, Olukemi 

Rahim-Awab, Ghulam 

Barnadas, Celine 

Berry, Antoine 

Boum, Yap 

Bustos, Maria D 

Cao, Jun 

Chen, Jun-Hu 

Collet, Louis 

Cui, Liwang 

Thakur, Garib-Das 

Dieye, Alioune 

Djalle, Djibrine 

Dorkenoo, Monique A 

Eboumbou-Moukoko, Carole E 

Espino, Fe-Esperanza-Caridad J 

Fandeur, Thierry 

Ferreira-da-Cruz, Maria-Fatima 

Fola, Abebe A 

Fuehrer, Hans-Peter 

Hassan, Abdillahi M 

Herrera, Socrates 

Hongvanthong, Bouasy 

Houze, Sandrine 

Ibrahim, Maman L 

Jahirul-Karim, Mohammad 

Jiang, Lubin 

Kano, Shigeyuki 

Ali-Khan, Wasif 

Khanthavong, Maniphone 

Kremsner, Peter G 

Lacerda, Marcus 

Leang, Rithea 

Leelawong, Mindy 

Li, Mei 

Lin, Khin 

Mazarati, Jean-Baptiste 

Menard, Sandie 

Morlais, Isabelle 

Muhindo-Mavoko, Hypolite 

Musset, Lise 

Na-Bangchang, Kesara 

Nambozi, Michael 

Niare, Karamoko 

Noedl, Harald 

Ouedraogo, Jean-Bosco 

Pillai, Dylan R 

Pradines, Bruno 

Quang-Phuc, Bui 

Ramharter, Michael 

Randrianarivelojosia, Milijaona 

Sattabongkot, Jetsumon 

Sheikh-Omar, Abdiqani 

Silue, Kigbafori D 

Sirima, Sodiomon B 

Sutherland, Colin 

Syafruddin, Din 

Tahar, Rachida 

Tang, Lin-Hua 

Toure, Offianan A 

Tshibangu-wa-Tshibangu, Patrick 

Vigan-Womas, Ines 

Warsame, Marian 

Wini, Lyndes 

Zakeri, Sedigheh 

Kim, Saorin 

Eam, Rotha 

Berne, Laura 

Khean, Chanra 

Chy, Sophy 

Ken, Malen 

Loch, Kaknika 

Canier, Lydie 

Duru, Valentine 

Legrand, Eric 

Barale, Jean-Christophe 

Stokes, Barbara 

Straimer, Judith 

Witkowski, Benoit 

Fidock, David A 

Rogier, Christophe 

Ringwald, Pascal 

Ariey, Frederic 

Mercereau-Puijalon, Odile 

KARMA Consortium 

AI109023/AI/NIAID NIH HHS/ 

T32 AI106711/AI/NIAID NIH HHS/ 

U19AI089702/AI/NIAID NIH HHS/ 

U19AI089672/AI/NIAID NIH HHS/ 

R01 AI109023/AI/NIAID NIH HHS/ 

R01 AI11646601/AI/NIAID NIH HHS/ 

D43 TW007393/TW/FIC NIH HHS/ 

U19 AI089672/AI/NIAID NIH HHS/ 

U19 AI089702/AI/NIAID NIH HHS/ 

N Engl J Med. 2016 Jun 23;374(25):2453-64. doi: 10.1056/NEJMoa1513137.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Insight into k13-propeller gene polymorphism and ex vivo DHA-response profiles from Cameroonian isolates},

author = {Menard, S. and Tchoufack, J. N. and Maffo, C. N. and Nsango, S. E. and Iriart, X. and Abate, L. and Tsapi, M. T. and Awono-Ambene, P. H. and Abega Mekongo, F. A. and Morlais, I. and Berry, A.},

year  = {2016},

date = {2016-01-01},

journal = {Malar J},

volume = {15},

number = {1},

pages = {572},

abstract = {BACKGROUND: The spread of Plasmodium falciparum resistance to artemisinin derivatives in Southeast Asia is a major source of concern and the emergence of resistance in Africa would have dramatic consequences, by increasing malaria mortality and morbidity. It is therefore urgent to implement regular monitoring in sentinel sites in sub-Saharan Africa using robust and easy-to-implement tools. The prevalence of k13-propeller mutations and the phenotypic profiles are poorly known in sub-Saharan Africa. Here, the k13-propeller polymorphism was compared to both ex vivo susceptibility to DHA and early parasitological and clinical responses to artemisinin combination therapy (ACT). METHODS: Plasmodium falciparum isolates were collected in 2015 in Yaounde (Cameroon) from patients treated with dihydroartemisinin-piperaquine combination. Samples were analysed for their susceptibility to artemisinin using the k13-propeller sequencing, the ex vivo ring-stage survival assay, the in vivo parasite positive rate and the clinical statute at day 2. RESULTS: None of the collected isolates revealed the presence of resistance mutations in the k13-propeller sequence. The median ring-stage survival rate for all the 64 interpretable isolates after a 6-hour pulse of 700 nM dihydroartemisinin was low, 0.49% (IQR: 0-1.3). Total parasite clearance was observed for 87.5% of patients and the remaining parasitaemic isolates (12.5%) showed a high reduction of parasite load, ranging from 97.5 to 99.9%. Clinical symptoms disappeared in 92.8% of cases. CONCLUSION: This study demonstrated the absence of k13-resistant genotypes in P. falciparum isolates from Cameroon. Only synonymous mutations were found with a low prevalence (4.3%). A good association between k13 genotypes and the ex vivo ring-stage survival assay or parasitological and clinical data was obtained. These results give a baseline for the long-term monitoring of artemisinin derivative efficacy in Africa.},

note = {Menard, Sandie 

Tchoufack, Joelle Njila 

Maffo, Christelle Ngou 

Nsango, Sandrine E 

Iriart, Xavier 

Abate, Luc 

Tsapi, Majoline Tchioffo 

Awono-Ambene, Parfait H 

Abega Mekongo, Francis A 

Morlais, Isabelle 

Berry, Antoine 

England 

Malar J. 2016 Nov 26;15(1):572.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Transnuclear CD8 T cells specific for the immunodominant epitope Gra6 lower acute-phase Toxoplasma gondii burden},

author = {Sanecka, A. and Yoshida, N. and Dougan, S. K. and Jackson, J. and Shastri, N. and Ploegh, H. and Blanchard, N. and Frickel, E. M.},

year  = {2016},

date = {2016-01-01},

journal = {Immunology},

abstract = {We generated a CD8 T-cell receptor (TCR) transnuclear (TN) mouse specific to the Ld -restricted immunodominant epitope of GRA6 from Toxoplasma gondii as a source of cells to facilitate further investigation into the CD8 T-cell-mediated response against this pathogen. The TN T cells bound Ld -Gra6 tetramer and proliferated upon unspecific and peptide-specific stimulation. The TCR beta sequence of the Gra6-specific TN CD8 T cells is identical in its V- and J-region to the TCR-beta harboured by a hybridoma line generated in response to Gra6 peptide. Adoptively transferred Gra6 TN CD8 T cells proliferated upon Toxoplasma infection in vivo and exhibited an activated phenotype similar to host CD8 T cells specific to Gra6. The brain of Toxoplasma-infected mice carried Gra6 TN cells already at day 8 post-infection. Both Gra6 TN mice as well as adoptively transferred Gra6 TN cells were able to significantly reduce the parasite burden in the acute phase of Toxoplasma infection. Overall, the Gra6 TN mouse represents a functional tool to study the protective and immunodominant specific CD8 T-cell response to Toxoplasma in both the acute and the chronic phases of infection.},

note = {Sanecka, Anna 

Yoshida, Nagisa 

Dougan, Stephanie K 

Jackson, John 

Shastri, Nilabh 

Ploegh, Hidde 

Blanchard, Nicolas 

Frickel, Eva-Maria 

Immunology. 2016 Jul 5. doi: 10.1111/imm.12643.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {An epidemiologically successful Escherichia coli sequence type modulates Plasmodium falciparum infection in the mosquito midgut},

author = {Tchioffo, M. T. and Abate, L. and Boissiere, A. and Nsango, S. E. and Gimonneau, G. and Berry, A. and Oswald, E. and Dubois, D. and Morlais, I.},

year  = {2016},

date = {2016-01-01},

journal = {Infect Genet Evol},

volume = {43},

pages = {22-30},

abstract = {Malaria transmission relies on the successful development of Plasmodium parasites in the Anopheles mosquito vector. Within the mosquito midgut, malaria parasites encounter a resident bacterial flora and parasite-bacteria interactions modulate Plasmodium development. The mechanisms by which the bacteria interact with malaria parasites are still unknown. The intestinal microbiota could regulate immune signaling pathways or produce bacterial compounds that block Plasmodium development. In this study, we characterized Escherichia coli strains previously isolated from the Anopheles mosquito midgut and investigated the putative role of two E. coli clones, 444ST95 and 351ST73, on parasite development. Sporogonic development was significantly impacted by exposure to clone 444ST95 whereas prevalence and intensity of infection were not different in mosquitoes challenged with 351ST73 as compared to control mosquitoes. This result indicates midgut bacteria exhibit intra-specific variation in their ability to inhibit Plasmodium development. Expression patterns of immune genes differed between mosquitoes challenged with 444ST95 and 351ST73 and examination of the luminal midgut surface by transmission electron microscopy revealed distinct effects of bacterial exposure on midgut epithelial cells. The 444ST95 clone strongly affected mosquito survival and parasite development and this could be associated to the Hemolysin F or other toxins released by the bacteria. Further studies will be needed to decipher the virulence factors and to determine their contribution to the observed phenotype of the 444ST95E. coli strain that belongs to the epidemiological ST95 clonal group responsible for extra intestinal infections in human and other animals.},

note = {Tchioffo, Majoline T 

Abate, Luc 

Boissiere, Anne 

Nsango, Sandrine E 

Gimonneau, Geoffrey 

Berry, Antoine 

Oswald, Eric 

Dubois, Damien 

Morlais, Isabelle 

Netherlands 

Infect Genet Evol. 2016 Sep;43:22-30. doi: 10.1016/j.meegid.2016.05.002. Epub 2016 May 3.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Rab22a controls MHC-I intracellular trafficking and antigen cross-presentation by dendritic cells},

author = {Cebrian, I. and Croce, C. and Guerrero, N. A. and Blanchard, N. and Mayorga, L. S.},

year  = {2016},

date = {2016-01-01},

journal = {EMBO Rep},

abstract = {Cross-presentation by MHC class I molecules allows the detection of exogenous antigens by CD8+ T lymphocytes. This process is crucial to initiate cytotoxic immune responses against many pathogens (i.e., Toxoplasma gondii) and tumors. To achieve efficient cross-presentation, dendritic cells (DCs) have specialized endocytic pathways; however, the molecular effectors involved are poorly understood. In this work, we identify the small GTPase Rab22a as a key regulator of MHC-I trafficking and antigen cross-presentation by DCs. Our results demonstrate that Rab22a is recruited to DC endosomes and phagosomes, as well as to the vacuole containing T. gondii parasites. The silencing of Rab22a expression did not affect the uptake of exogenous antigens or parasite invasion, but it drastically reduced the intracellular pool and the recycling of MHC-I molecules. The knockdown of Rab22a also hampered the cross-presentation of soluble, particulate and T. gondii-associated antigens, but not the endogenous MHC-I antigen presentation through the classical secretory pathway. Our findings provide compelling evidence that Rab22a plays a central role in the MHC-I endocytic trafficking, which is crucial for efficient cross-presentation by DCs.},

note = {Oct 10. pii: e201642358.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Continuous Effector CD8(+) T Cell Production in a Controlled Persistent Infection Is Sustained by a Proliferative Intermediate Population},

author = {Chu, H. H. and Chan, S. W. and Gosling, J. P. and Blanchard, N. and Tsitsiklis, A. and Lythe, G. and Shastri, N. and Molina-Paris, C. and Robey, E. A.},

year  = {2016},

date = {2016-01-01},

journal = {Immunity},

volume = {45},

number = {1},

pages = {159-71},

abstract = {Highly functional CD8(+) effector T (Teff) cells can persist in large numbers during controlled persistent infections, as exemplified by rare HIV-infected individuals who control the virus. Here we examined the cellular mechanisms that maintain ongoing T effector responses using a mouse model for persistent Toxoplasma gondii infection. In mice expressing the protective MHC-I molecule, H-2L(d), a dominant T effector response against a single parasite antigen was maintained without a contraction phase, correlating with ongoing presentation of the dominant antigen. Large numbers of short-lived Teff cells were continuously produced via a proliferative, antigen-dependent intermediate (Tint) population with a memory-effector hybrid phenotype. During an acute, resolved infection, decreasing antigen load correlated with a sharp drop in the Tint cell population and subsequent loss of the ongoing effector response. Vaccination approaches aimed at the development of Tint populations might prove effective against pathogens that lead to chronic infection.},

note = {Jul 19;45(1):159-71. doi: 10.1016/j.immuni.2016.06.013. Epub 2016 Jul 12.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {Erythroferrone contributes to hepcidin repression in a mouse model of malarial anemia},

author = {Latour, C. and Wlodarczyk, M. F. and Jung, G. and Gineste, A. and Blanchard, N. and Ganz, T. and Roth, M. P. and Coppin, H. and Kautz, L.},

year  = {2016},

date = {2016-01-01},

journal = {Haematologica},

abstract = {Malaria, a major global health challenge worldwide, is accompanied by a severe anemia secondary to hemolysis and increased erythrophagocytosis. Iron is an essential functional component of erythrocyte hemoglobin and its availability is controlled by the liver-derived hormone hepcidin. We examined the regulation of hepcidin during malarial infection in mice using the rodent parasite Plasmodium berghei K173 (PbK). Mice infected with PbK develop a severe anemia and die after 18 to 22 days without cerebral malaria. During the early phase of blood-stage infection (day 1 to 5), a strong inflammatory signature was associated with increased production of hepcidin. Between days 7 and 18, while infection progresses, red blood cell count, hemoglobin and hematocrit dramatically decreased. In the late phase of malarial infection, hepcidin production was reduced concomitantly to an increase in the mRNA expression of the hepcidin suppressor erythroferrone (ERFE) in the bone marrow and the spleen. Compared with wild-type mice, Erfe-/- mice failed to adequately suppress hepcidin expression after infection with PbK. Importantly, the sustained production of hepcidin allowed by ERFE ablation was associated with decreased parasitemia, providing further evidence that transient iron restriction could be beneficial in the treatment of malaria.},

note = {Sep 22. pii: haematol.2016.150227.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{b,

title = {A Worldwide Map of Plasmodium falciparum K13-Propeller Polymorphisms},

author = {Menard, D. and Khim, N. and Beghain, J. and Adegnika, A. A. and Shafiul-Alam, M. and Amodu, O. and Rahim-Awab, G. and Barnadas, C. and Berry, A. and Boum, Y. and Bustos, M. D. and Cao, J. and Chen, J. H. and Collet, L. and Cui, L. and Thakur, G. D. and Dieye, A. and Djalle, D. and Dorkenoo, M. A. and Eboumbou-Moukoko, C. E. and Espino, F. E. and Fandeur, T. and Ferreira-da-Cruz, M. F. and Fola, A. A. and Fuehrer, H. P. and Hassan, A. M. and Herrera, S. and Hongvanthong, B. and Houze, S. and Ibrahim, M. L. and Jahirul-Karim, M. and Jiang, L. and Kano, S. and Ali-Khan, W. and Khanthavong, M. and Kremsner, P. G. and Lacerda, M. and Leang, R. and Leelawong, M. and Li, M. and Lin, K. and Mazarati, J. B. and Menard, S. and Morlais, I. and Muhindo-Mavoko, H. and Musset, L. and Na-Bangchang, K. and Nambozi, M. and Niare, K. and Noedl, H. and Ouedraogo, J. B. and Pillai, D. R. and Pradines, B. and Quang-Phuc, B. and Ramharter, M. and Randrianarivelojosia, M. and Sattabongkot, J. and Sheikh-Omar, A. and Silue, K. D. and Sirima, S. B. and Sutherland, C. and Syafruddin, D. and Tahar, R. and Tang, L. H. and Toure, O. A. and Tshibangu-wa-Tshibangu, P. and Vigan-Womas, I. and Warsame, M. and Wini, L. and Zakeri, S. and Kim, S. and Eam, R. and Berne, L. and Khean, C. and Chy, S. and Ken, M. and Loch, K. and Canier, L. and Duru, V. and Legrand, E. and Barale, J. C. and Stokes, B. and Straimer, J. and Witkowski, B. and Fidock, D. A. and Rogier, C. and Ringwald, P. and Ariey, F. and Mercereau-Puijalon, O.},

year  = {2016},

date = {2016-01-01},

journal = {N Engl J Med},

volume = {374},

number = {25},

pages = {2453-64},

abstract = {BACKGROUND: Recent gains in reducing the global burden of malaria are threatened by the emergence of Plasmodium falciparum resistance to artemisinins. The discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domains are the major determinant of resistance has provided opportunities for monitoring such resistance on a global scale. METHODS: We analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic. Most of the samples (84.5%) were obtained from patients who were treated at sentinel sites used for nationwide surveillance of antimalarial resistance. We evaluated the emergence and dissemination of mutations by haplotyping neighboring loci. RESULTS: We identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution. In Asia, 36.5% of the K13 mutations were distributed within two areas--one in Cambodia, Vietnam, and Laos and the other in western Thailand, Myanmar, and China--with no overlap. In Africa, we observed a broad array of rare nonsynonymous mutations that were not associated with delayed parasite clearance. The gene-edited Dd2 transgenic line with the A578S mutation, which expresses the most frequently observed African allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay. CONCLUSIONS: No evidence of artemisinin resistance was found outside Southeast Asia and China, where resistance-associated K13 mutations were confined. The common African A578S allele was not associated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neutral. (Funded by Institut Pasteur Paris and others.).},

note = {Jun 23;374(25):2453-64. doi: 10.1056/NEJMoa1513137.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}