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Nature Immunology

Masaru Kanekiyo, M Gordon Joyce, Rebecca A Gillespie, John R Gallagher, Sarah F Andrews, Hadi M Yassine, Adam K Wheatley, Brian E Fisher, David R Ambrozak, Adrian Creanga, Kwanyee Leung, Eun Sung Yang, Seyhan Boyoglu-Barnum, Ivelin S Georgiev, Yaroslav Tsybovsky, Madhu S Prabhakaran, Hanne Andersen, Wing-Pui Kong, Ulrich Baxa, Kathryn L Zephir, Julie E Ledgerwood, Richard A Koup, Peter D Kwong, Audray K Harris, Adrian B McDermott, John R Mascola, Barney S Graham
The present vaccine against influenza virus has the inevitable risk of antigenic discordance between the vaccine and the circulating strains, which diminishes vaccine efficacy. This necessitates new approaches that provide broader protection against influenza. Here we designed a vaccine using the hypervariable receptor-binding domain (RBD) of viral hemagglutinin displayed on a nanoparticle (np) able to elicit antibody responses that neutralize H1N1 influenza viruses spanning over 90 years. Co-display of RBDs from multiple strains across time, so that the adjacent RBDs are heterotypic, provides an avidity advantage to cross-reactive B cells...
February 11, 2019: Nature Immunology
Florian Krammer
No abstract text is available yet for this article.
February 11, 2019: Nature Immunology
Ziv Erlich, Inbar Shlomovitz, Liat Edry-Botzer, Hadar Cohen, Daniel Frank, Hanqing Wang, Andrew M Lew, Kate E Lawlor, Yifan Zhan, James E Vince, Motti Gerlic
Inflammasomes are one of the most important mechanisms for innate immune defense against microbial infection but are also known to drive various inflammatory disorders via processing and release of the cytokine IL-1β. As research into the regulation and effects of inflammasomes in disease has rapidly expanded, a variety of cell types, including dendritic cells (DCs), have been suggested to be inflammasome competent. Here we describe a major fault in the widely used DC-inflammasome model of bone marrow-derived dendritic cells (BMDCs) generated with the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF)...
February 11, 2019: Nature Immunology
Ai Ing Lim, Oliver J Harrison, Yasmine Belkaid
No abstract text is available yet for this article.
February 11, 2019: Nature Immunology
Leona Gabryšová, Marisol Alvarez-Martinez, Raphaëlle Luisier, Luke S Cox, Jan Sodenkamp, Caroline Hosking, Damián Pérez-Mazliah, Charlotte Whicher, Yashaswini Kannan, Krzysztof Potempa, Xuemei Wu, Leena Bhaw, Hagen Wende, Michael H Sieweke, Greg Elgar, Mark Wilson, James Briscoe, Vicki Metzis, Jean Langhorne, Nicholas M Luscombe, Anne O'Garra
In the version of this article initially published, the Supplementary Data file was an incorrect version. The correct version is now provided. The error has been corrected in the HTML and PDF version of the article.
February 8, 2019: Nature Immunology
Jamie R J Inshaw, Antony J Cutler, Oliver S Burren, M Irina Stefana, John A Todd
In the version of this article initially published, the bibliographic information for reference 2 was incorrect in the reference list, and reference 2 was cited incorrectly at the end of the second sentence in the second paragraph ("...were identified2 ."). The correct reference 2 is as follows: "Kong, A. et al. The nature of nurture: Effects of parental genotypes. Science 359, 424-428 (2018)." The reference that should be cited at the end of the aforementioned sentence, which should be numbered '5' ("...
February 7, 2019: Nature Immunology
Ayano C Kohlgruber, Shani T Gal-Oz, Nelson M LaMarche, Moto Shimazaki, Danielle Duquette, Hui-Fern Koay, Hung N Nguyen, Amir I Mina, Tyler Paras, Ali Tavakkoli, Ulrich von Andrian, Adam P Uldrich, Dale I Godfrey, Alexander S Banks, Tal Shay, Michael B Brenner, Lydia Lynch
In the version of this article initially published, three authors (Hui-Fern Kuoy, Adam P. Uldrich and Dale. I. Godfrey) and their affiliations, acknowledgments and contributions were not included. The correct information is as follows:Ayano C. Kohlgruber1,2 , Shani T. Gal-Oz3 , Nelson M. LaMarche1,2 , Moto Shimazaki1 , Danielle Duquette4 , Hui-Fern Koay5,6 , Hung N. Nguyen1 , Amir I. Mina4 , Tyler Paras1 , Ali Tavakkoli7 , Ulrich von Andrian2,8 , Adam P. Uldrich5,6 , Dale I. Godfrey5,6 , Alexander S. Banks4 , Tal Shay3 , Michael B...
February 7, 2019: Nature Immunology
Jake Dunning, Simon Blankley, Long T Hoang, Mike Cox, Christine M Graham, Philip L James, Chloe I Bloom, Damien Chaussabel, Jacques Banchereau, Stephen J Brett, Miriam F Moffatt, Anne O'Garra, Peter J M Openshaw
In the version of this article initially published, a source of funding was not included in the Acknowledgements section. That section should include the following: P.J.M.O. was supported by EU FP7 PREPARE project 602525. The error has been corrected in the HTML and PDF version of the article.
February 7, 2019: Nature Immunology
Toshiyuki Fukada, Shintaro Hojyo, Takafumi Hara, Teruhisa Takagishi
No abstract text is available yet for this article.
February 4, 2019: Nature Immunology
David K Finlay
No abstract text is available yet for this article.
February 4, 2019: Nature Immunology
Consuelo Anzilotti, David J Swan, Bertrand Boisson, Mukta Deobagkar-Lele, Catarina Oliveira, Pauline Chabosseau, Karin R Engelhardt, Xijin Xu, Rui Chen, Luis Alvarez, Rolando Berlinguer-Palmini, Katherine R Bull, Eleanor Cawthorne, Adam P Cribbs, Tanya L Crockford, Tarana Singh Dang, Amy Fearn, Emma J Fenech, Sarah J de Jong, B Christoffer Lagerholm, Cindy S Ma, David Sims, Bert van den Berg, Yaobo Xu, Andrew J Cant, Gary Kleiner, T Ronan Leahy, M Teresa de la Morena, Jennifer M Puck, Ralph S Shapiro, Mirjam van der Burg, J Ross Chapman, John C Christianson, Benjamin Davies, John A McGrath, Stefan Przyborski, Mauro Santibanez Koref, Stuart G Tangye, Andreas Werner, Guy A Rutter, Sergi Padilla-Parra, Jean-Laurent Casanova, Richard J Cornall, Mary Ellen Conley, Sophie Hambleton
Despite the known importance of zinc for human immunity, molecular insights into its roles have remained limited. Here we report a novel autosomal recessive disease characterized by absent B cells, agammaglobulinemia and early onset infections in five unrelated families. The immunodeficiency results from hypomorphic mutations of SLC39A7, which encodes the endoplasmic reticulum-to-cytoplasm zinc transporter ZIP7. Using CRISPR-Cas9 mutagenesis we have precisely modeled ZIP7 deficiency in mice. Homozygosity for a null allele caused embryonic death, but hypomorphic alleles reproduced the block in B cell development seen in patients...
February 4, 2019: Nature Immunology
Zhenke Wen, Ke Jin, Yi Shen, Zhen Yang, Yinyin Li, Bowen Wu, Lu Tian, Stanford Shoor, Niall E Roche, Jorg J Goronzy, Cornelia M Weyand
N-myristoyltransferase (NMT) attaches the fatty acid myristate to the N-terminal glycine of proteins to sort them into soluble and membrane-bound fractions. Function of the energy-sensing AMP-activated protein kinase, AMPK, is myristoylation dependent. In rheumatoid arthritis (RA), pathogenic T cells shift glucose away from adenosine tri-phosphate production toward synthetic and proliferative programs, promoting proliferation, cytokine production, and tissue invasion. We found that RA T cells had a defect in NMT1 function, which prevented AMPK activation and enabled unopposed mTORC1 signaling...
February 4, 2019: Nature Immunology
Devin Sok, Dennis R Burton
In the version of this article initially published, some of the references in Table 1 were incorrect. The correct references are as follows: in row 12, refs. 12,44 should be ref. 12; in row 16, refs. 2,17,27 should be ref. 109 (Walker, L. M. et al. Broad neutralization coverage of HIV by multiple highly potent antibodies. Nature 477, 466-470 (2011)); in row 25, refs. 61,76 should be ref. 110 (Wu, X. et al. Rational design of envelope identifies broadly neutralizing human monoclonal antibodies to HIV-1. Science 329, 856-861 (2010)); and in the bottom row, ref...
February 1, 2019: Nature Immunology
Aisling O'Hara Hall, Jennifer E Towne, Scott E Plevy
In the version of this article initially published, a word ("neutraling") in sentence 2 of paragraph 5 is incorrect. The correct phrase is "...neutralizing properties...". The error has been corrected in the HTML and PDF version of the article.
February 1, 2019: Nature Immunology
Youn Jung Choi, Stephanie Kim, Younho Choi, Travis B Nielsen, Jun Yan, Alvin Lu, Jianbin Ruan, Hye-Ra Lee, Hao Wu, Brad Spellberg, Jae U Jung
Inflammatory caspases (caspase-1, caspase-4, caspase-5 and caspase-11 (caspase-1/-4/-5/-11)) mediate host defense against microbial infections, processing pro-inflammatory cytokines and triggering pyroptosis. However, precise checkpoints are required to prevent their unsolicited activation. Here we report that serpin family B member 1 (SERPINB1) limited the activity of those caspases by suppressing their caspase-recruitment domain (CARD) oligomerization and enzymatic activation. While the reactive center loop of SERPINB1 inhibits neutrophil serine proteases, its carboxy-terminal CARD-binding motif restrained the activation of pro-caspase-1/-4/-5/-11...
January 28, 2019: Nature Immunology
Sebastian Zundler, Emily Becker, Marta Spocinska, Monique Slawik, Loreto Parga-Vidal, Regina Stark, Maximilian Wiendl, Raja Atreya, Timo Rath, Moritz Leppkes, Kai Hildner, Rocío López-Posadas, Sören Lukassen, Arif B Ekici, Clemens Neufert, Imke Atreya, Klaas P J M van Gisbergen, Markus F Neurath
Although tissue-resident memory T cells (TRM cells) have been shown to regulate host protection in infectious disorders, their function in inflammatory bowel disease (IBD) remains to be investigated. Here we characterized TRM cells in human IBD and in experimental models of intestinal inflammation. Pro-inflammatory TRM cells accumulated in the mucosa of patients with IBD, and the presence of CD4+ CD69+ CD103+ TRM cells was predictive of the development of flares. In vivo, functional impairment of TRM cells in mice with double knockout of the TRM -cell-associated transcription factors Hobit and Blimp-1 attenuated disease in several models of colitis, due to impaired cross-talk between the adaptive and innate immune system...
January 28, 2019: Nature Immunology
Mingen Liu, Roddy S O'Connor, Sophie Trefely, Kathleen Graham, Nathaniel W Snyder, Gregory L Beatty
Macrophages enforce antitumor immunity by engulfing and killing tumor cells. Although these functions are determined by a balance of stimulatory and inhibitory signals, the role of macrophage metabolism is unknown. Here, we study the capacity of macrophages to circumvent inhibitory activity mediated by CD47 on cancer cells. We show that stimulation with a CpG oligodeoxynucleotide, a Toll-like receptor 9 agonist, evokes changes in the central carbon metabolism of macrophages that enable antitumor activity, including engulfment of CD47+ cancer cells...
January 21, 2019: Nature Immunology
Na Li, Vincent van Unen, Tamim Abdelaal, Nannan Guo, Sofya A Kasatskaya, Kristin Ladell, James E McLaren, Evgeny S Egorov, Mark Izraelson, Susana M Chuva de Sousa Lopes, Thomas Höllt, Olga V Britanova, Jeroen Eggermont, Noel F C C de Miranda, Dmitriy M Chudakov, David A Price, Boudewijn P F Lelieveldt, Frits Koning
The fetus is thought to be protected from exposure to foreign antigens, yet CD45RO+ T cells reside in the fetal intestine. Here we combined functional assays with mass cytometry, single-cell RNA sequencing and high-throughput T cell antigen receptor (TCR) sequencing to characterize the CD4+ T cell compartment in the human fetal intestine. We identified 22 CD4+ T cell clusters, including naive-like, regulatory-like and memory-like subpopulations, which were confirmed and further characterized at the transcriptional level...
January 21, 2019: Nature Immunology
Billur Akkaya, Yoshihiro Oya, Munir Akkaya, Jafar Al Souz, Amanda H Holstein, Olena Kamenyeva, Juraj Kabat, Ryutaro Matsumura, David W Dorward, Deborah D Glass, Ethan M Shevach
Regulatory T cells (Treg cells) can activate multiple suppressive mechanisms in vitro after activation via the T cell antigen receptor, resulting in antigen-independent suppression. However, it remains unclear whether similar pathways operate in vivo. Here we found that antigen-specific Treg cells activated by dendritic cells (DCs) pulsed with two antigens suppressed conventional naive T cells (Tnaive cells) specific for both cognate antigens and non-cognate antigens in vitro but suppressed only Tnaive cells specific for cognate antigen in vivo...
January 14, 2019: Nature Immunology
David L Owen, Shawn A Mahmud, Louisa E Sjaastad, Jason B Williams, Justin A Spanier, Dimitre R Simeonov, Roland Ruscher, Weishan Huang, Irina Proekt, Corey N Miller, Can Hekim, Jonathan C Jeschke, Praful Aggarwal, Ulrich Broeckel, Rebecca S LaRue, Christine M Henzler, Maria-Luisa Alegre, Mark S Anderson, Avery August, Alexander Marson, Ye Zheng, Calvin B Williams, Michael A Farrar
The developmental programs that generate a broad repertoire of regulatory T cells (Treg cells) able to respond to both self antigens and non-self antigens remain unclear. Here we found that mature Treg cells were generated through two distinct developmental programs involving CD25+ Treg cell progenitors (CD25+ Treg P cells) and Foxp3lo Treg cell progenitors (Foxp3lo Treg P cells). CD25+ Treg P cells showed higher rates of apoptosis and interacted with thymic self antigens with higher affinity than did Foxp3lo Treg P cells, and had a T cell antigen receptor repertoire and transcriptome distinct from that of Foxp3lo Treg P cells...
January 14, 2019: Nature Immunology
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