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Nature Immunology Contents: January 2017 Volume 18 pp 1 - 113

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TABLE OF CONTENTS

January 2017 Volume 18, Issue 1

Meeting Report
News and Views
Research Highlights
Articles


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Innate Immune Memory (14-16 March 2017) 

This conference will focus on the adaptive features of the innate immune system and how it can be activated and regulated, as well as how it can be 'trained' by internal and external modulators and how this might be harnessed to develop new therapies.

Deadlines: Bursary: 17 Jan 2017/ Abstracts: 31 Jan / Registration: 15 Feb
 

Meeting Report

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1st International Conference on Human & Translational Immunology   pp1 - 4
Jennifer L Hope, Bali Pulendran, Stephen P Schoenberger and Peter D Katsikis
doi:10.1038/ni.3635

News and Views

Top

Linking air pollution to atopic dermatitis   pp5 - 6
Kenji Kabashima, Atsushi Otsuka and Takashi Nomura
doi:10.1038/ni.3615
The relationship between atopic dermatitis and air pollution has been long debated but has now been connected via the aryl hydrocarbon receptor and its control of skin innervation and the consequent triggering of an itch-scratch response.

See also: Article by Hidaka et al.

Finding the 'ubiquitous' threads in infection and autoimmune neuroinflammation   pp7 - 8
Sophia Bardehle, Victoria Rafalski and Katerina Akassoglou
doi:10.1038/ni.3633
The deubiquitinase USP15 acts with the ubiquitin ligase TRIM25 to activate a type I interferon response and exacerbate microbial and autoimmune neuroinflammation.

See also: Article by Torre et al.

Old dog, new tricks: IL-6 cluster signaling promotes pathogenic TH17 cell differentiation   pp8 - 10
Francisco J Quintana
doi:10.1038/ni.3637
Different cellular sources and signaling mechanisms mediate the effects of IL-6 on the generation of pathogenic TH17 helper T cells and the suppression of Foxp3+ regulatory T cells.

See also: Article by Heink et al.

iNKT cells do a fat lot of good   pp10 - 12
Jayati Mookerjee-Basu and Dietmar J Kappes
doi:10.1038/ni.3639
Altered signaling via the T cell antigen receptor (TCR) promotes an adipose-tissue-like phenotype in invariant natural killer cells (iNKT cells) during thymic development and causes selective enrichment for iNKT cells in adipose tissues.

See also: Article by Vieth et al.

How lymphocytes add up   pp12 - 13
Becca Asquith and Rob J de Boer
doi:10.1038/ni.3636
A surprising molecular mechanism underlying signal integration and programmed proliferation in adaptive immunity has been identified: the cell-cycle regulator Myc enables a lymphocyte to add up the strength of signals it receives and time its response accordingly.

See also: Article by Heinzel et al.

Immunology
JOBS of the week
Postdoc with focus on pre-clinical in vivo studies and immunology
German Cancer Research Center (DKFZ).
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University of Toronto
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University of Massachusetts
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University of Georgia, College of Veterinary Medicine
Two Junior Group Leader Positions
Centre for Genomic Regulation
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Fundamental Immunology Its Therapeutic Potential
25.04.17
Cold Spring Harbor, USA
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Research Highlights

Top

Apoptosis footprint | Counting HSCs | Clearing liver metastases | Motile recognition | CD148 function in B-1 cells | TSLP in bacterial skin infection

Articles

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Gradients of the signaling lipid S1P in lymph nodes position natural killer cells and regulate their interferon-γ response   pp15 - 25
Victoria Fang, V Sai Chaluvadi, Willy D Ramos-Perez, Alejandra Mendoza, Audrey Baeyens et al.
doi:10.1038/ni.3619
Natural killer cells are a rapid source of the cytokine IFN-γ that influences ensuing immune responses. Schwab and colleagues report that gradients of the signaling lipid S1P regulate the positioning of natural killer cells in lymph nodes necessary for this response.

The signaling adaptor TRAF1 negatively regulates Toll-like receptor signaling and this underlies its role in rheumatic disease   pp26 - 35
Ali A Abdul-Sater, Maria I Edilova, Derek L Clouthier, Achire Mbanwi, Elisabeth Kremmer et al.
doi:10.1038/ni.3618
The signaling adaptor TRAF1 is involved in TNFR-induced survival. Watts and colleagues demonstrate that TRAF1 also negatively regulates NF-κB activation by interfering with linear ubiquitination of the signaling subunit NEMO.

TCRα-TCRβ pairing controls recognition of CD1d and directs the development of adipose NKT cells   pp36 - 44
Joshua A Vieth, Joy Das, Fanomezana M Ranaivoson, Davide Comoletti, Lisa K Denzin et al.
doi:10.1038/ni.3622
Sant'Angelo and colleagues show that disruption of a hydrophobic patch in the T cell antigen receptor on natural killer T cells alters their development, which results in the selective accumulation of adipose-tissue-specific natural killer T cells.

See also: News and Views by Mookerjee-Basu & Kappes

TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells   pp45 - 53
Ageliki Tsagaratou, Edahí González-Avalos, Sini Rautio, James P Scott-Browne, Susan Togher et al.
doi:10.1038/ni.3630
TET proteins regulate 5-methylcytosine epigenetic marks, and thereby regulate chromatin accessibility. Rao and colleagues show that the combined loss of TET2 and TET3 in thymocytes skews development to iNKT17 cells as a result of upregulation of RORγt, which leads to lymphoproliferative disease and premature death.

USP15 regulates type I interferon response and is required for pathogenesis of neuroinflammation   pp54 - 63
Sabrina Torre, Maria J Polyak, David Langlais, Nassima Fodil, James M Kennedy et al.
doi:10.1038/ni.3581
Cerebral malaria infection can provoke fatal neuroinflammation. Gros and colleagues identify an ubiquitin-modification axis that exacerbates neuroinflammation and that involves TRIM25 and USP15, which jointly promote type I interferon production.

See also: News and Views by Bardehle et al.

The aryl hydrocarbon receptor AhR links atopic dermatitis and air pollution via induction of the neurotrophic factor artemin   pp64 - 73
Takanori Hidaka, Eisaku Ogawa, Eri H Kobayashi, Takafumi Suzuki, Ryo Funayama et al.
doi:10.1038/ni.3614
There are suspected links between air pollution and atopic dermatitis, but the mechanism has remained unclear. Yamamoto and colleagues demonstrate that air pollutants trigger activation of the aryl hydrocarbon receptor in the skin, hyperinnervation and an itch-scratch cycle that leads to atopic dermatitis.

See also: News and Views by Kabashima et al.

Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic TH17 cells   pp74 - 85
Sylvia Heink, Nir Yogev, Christoph Garbers, Marina Herwerth, Lilian Aly et al.
doi:10.1038/ni.3632
Korn and colleagues report that Sirpα+ dendritic cells trans-present the cytokine IL-6 to T cells through a process that requires its receptor IL-6Rα bound to dendritic cells and that trans-presentation is needed to generate pathogenic cells of the TH17 subset of helper T cells in vivo.

See also: News and Views by Quintana

A cycle of Zap70 kinase activation and release from the TCR amplifies and disperses antigenic stimuli   pp86 - 95
Zachary B Katz, Lucie Novotná, Amy Blount and Björn F Lillemeier
doi:10.1038/ni.3631
Lillemeier and colleagues describe a cycle of recruitment, activation and release of Zap70 kinase at phosphorylated T cell antigen receptors. According to this model, the receptor acts as a 'catalytic unit' that amplifies antigenic stimuli.

A Myc-dependent division timer complements a cell-death timer to regulate T cell and B cell responses   pp96 - 103
Susanne Heinzel, Tran Binh Giang, Andrey Kan, Julia M Marchingo, Bryan K Lye et al.
doi:10.1038/ni.3598
Lymphocytes integrate multiple input signals to regulate the extent of their proliferative response. Hodgkin and colleagues demonstrate that the proto-oncoprotein Myc is a cell-intrinsic division timer.

See also: News and Views by Asquith & de Boer

Regulation of autoantibody activity by the IL-23-TH17 axis determines the onset of autoimmune disease   pp104 - 113
Rene Pfeifle, Tobias Rothe, Natacha Ipseiz, Hans U Scherer, Stephan Culemann et al.
doi:10.1038/ni.3579
Kronke and colleagues show that the cytokine IL-23 controls the glycosylation profile and inflammatory activity of autoantibodies through control of sialyltransferase activity in plasma cells mediated by the TH17 subset of helper T cells.

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