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TABLE OF CONTENTS
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March 2017 Volume 18, Issue 3 |
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| News and Views Research Highlights Review Articles | |
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Nature Milestones: Antibodies
Nature Milestones: Antibodies chronicles the history of antibodies from their earliest description in antisera, their structure, generation and function, right through to their recent application in cancer immunotherapy. It also includes a timeline and a collection of seminal papers reproduced from Springer Nature.
Access the Milestone free online
Produced with support from BioLegend UCB | | | |
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News and Views | Top |
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Research Highlights | Top |
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Nuanced eosinophils | Inflammasomes in human aging | Neuroimmune interactions: ILC3s | Neuroimmune interactions: astrocytes | Anti-dengue IgG1 | CyTOF analysis of anti-tumor responses |
Review | Top |
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'Final common pathway' of human cancer immunotherapy: targeting random somatic mutations pp255 - 262 Eric Tran, Paul F Robbins and Steven A Rosenberg doi:10.1038/ni.3682 Rosenberg and colleagues review evidence suggesting that T cells that target tumor neoantigens arising from cancer mutations are the main mediators of many effective cancer immunotherapies in humans. |
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Articles | Top |
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The transcriptional regulator Aire binds to and activates super-enhancers pp263 - 273 Kushagra Bansal, Hideyuki Yoshida, Christophe Benoist and Diane Mathis doi:10.1038/ni.3675 Mathis and colleagues show that the transcriptional regulator Aire preferentially localizes in and activates super-enhancers. |
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Alternative pathway for the development of Vα14+ NKT cells directly from CD4-CD8- thymocytes that bypasses the CD4+CD8+ stage pp274 - 282 Nyambayar Dashtsoodol, Tomokuni Shigeura, Minako Aihara, Ritsuko Ozawa, Satoshi Kojo et al. doi:10.1038/ni.3668 Natural killer T cells (NKT cells) are thought to originate at the double-positive stage of thymopoiesis. Taniguchi and colleagues find that a subset of NKT cells also appear earlier, at the double-negative stage, and that these give rise to liver-resident NKT cells with highly potent effector function. |
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Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation pp283 - 292 Erez Dror, Elise Dalmas, Daniel T Meier, Stephan Wueest, Julien Thévenet et al. doi:10.1038/ni.3659 The cytokine IL-1β has well-established harmful effects on pancreatic islet function. Donath and colleagues identify an acute wave of postprandial IL-1β release and show that this unexpectedly has a positive effect on insulin secretion and the maintenance of normal metabolic function.
See also: News and Views by Hjorth & Febbraio |
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Chronic signaling via the metabolic checkpoint kinase mTORC1 induces macrophage granuloma formation and marks sarcoidosis progression pp293 - 302 Monika Linke, Ha Thi Thanh Pham, Karl Katholnig, Thomas Schnöller, Anne Miller et al. doi:10.1038/ni.3655 Macrophages are critical for granuloma formation, but the cell-intrinsic mechanisms remain unknown. Weichhart and colleagues demonstrate that chronic mTOR activity leads to macrophage-dependent granuloma formation, which may have relevance to sarcoidosis.
See also: News and Views by Pagan & Ramakrishnan |
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Gsk3 is a metabolic checkpoint regulator in B cells pp303 - 312 Julia Jellusova, Matthew H Cato, John R Apgar, Parham Ramezani-Rad, Charlotte R Leung et al. doi:10.1038/ni.3664 Mature B cells remain in a quiescent state until activated. Rickert and colleagues identify a prominent role for the kinase Gsk3 in resting naive B cells and in activated germinal center B cells that restrains the production of Myc and reactive oxygen species and prevents metabolic collapse. |
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Transitional B cells commit to marginal zone B cell fate by Taok3-mediated surface expression of ADAM10 pp313 - 320 Hamida Hammad, Matthias Vanderkerken, Philippe Pouliot, Kim Deswarte, Wendy Toussaint et al. doi:10.1038/ni.3657 The signaling receptor Notch is required for the generation of marginal zone B cells. Hammad and colleagues show that Notch signaling activates the kinase Taok3 and surface expression of the metalloproteinase ADAM10, which commits transitional B cells to the marginal zone B cell fate.
See also: News and Views by DeFranco |
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The IgM receptor FcμR limits tonic BCR signaling by regulating expression of the IgM BCR pp321 - 333 Trang T T Nguyen, Kathrin Kläsener, Christa Z&zuml;rn, Patricia A Castillo, Ingrid Brust-Mascher et al. doi:10.1038/ni.3677 FcμR serves as a receptor for soluble IgM. Baumgarth and colleagues show that intracellular FcμR constrains the surface expression of IgM. Lack of FcμR alters B cell populations and enhances autoantibody production. FcμR thereby serves as a critical regulator of B cell homeostasis. |
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Direct control of regulatory T cells by keratinocytes pp334 - 343 Mariko Kashiwagi, Junichi Hosoi, Jen-Feng Lai, Janice Brissette, Steven F Ziegler et al. doi:10.1038/ni.3661 Skin is constantly exposed to environmental stressors. Georgopoulos and colleagues show that regulatory T cells respond to the cytokine TSLP produced by stressed keratinocytes and that a loss of skin Treg cell expression of TSLPR leads to lethal inflammation. |
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The transcription factor musculin promotes the unidirectional development of peripheral Treg cells by suppressing the TH2 transcriptional program pp344 - 353 Chuan Wu, Zuojia Chen, Valerie Dardalhon, Sheng Xiao, Theresa Thalhamer et al. doi:10.1038/ni.3667 Transcription factors involved in consolidation of the induced regulatory T cell program are still being identified. Wu et al. demonstrate that the transcription factor musculin is critical for supporting the differentiation of these cells and prevents their acquisition of a T helper type 2 phenotype.
See also: News and Views by Pattarini & Soumelis |
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A sestrin-dependent Erk-Jnk-p38 MAPK activation complex inhibits immunity during aging pp354 - 363 Alessio Lanna, Daniel C O Gomes, Bojana Muller-Durovic, Thomas McDonnell, David Escors et al. doi:10.1038/ni.3665 Akbar, Lanna and colleagues show that sestrin proteins bind to and coordinate the simultaneous activation of Erk, Jnk and p38 MAPKs in T lymphocytes and inhibit immunity during aging. |
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