Friday, December 14, 2012

Nature Immunology Contents: January 2013 Volume 14 pp 1 - 99

Nature Immunology

Advertisement
Reichert is making it easier to have an SPR system installed in your lab today with this $4000 offer!
FREE Startup FREE Training FREE Fluidics Kit. A $4000 value.

Purchase any SPR system and receive free on-site setup and training.
Reichert SPR systems are ultra-sensitive and cost-effective for all biomolecular interaction analysis.
Visit website for details.
ReichertSPR.com
TABLE OF CONTENTS

January 2013 Volume 14, Issue 1

Meeting Report
Commentary
News and Views
Research Highlights
Review
Articles
Resource



Subscribe
 
Facebook
 
RSS
 
Recommend to library
 
Twitter
 
Advertisement
Nature Reviews Immunology
POSTER-THE IMMUNE RESPONSE TO HIV
Authors: Nina Bhardwaj, Florian Hladik and Susan Moir

www.nature.com/nri/posters/hiv

Produced with support from
STEMCELL Technologies
 

Meeting Report

Top

Antibody gene transfer for HIV immunoprophylaxis   pp1 - 5
Alejandro B Balazs and Anthony P West Jr
doi:10.1038/ni.2480

Commentary

Top

Job-search basics: how to convert a CV into a resume   pp6 - 9
Derek Haseltine
doi:10.1038/ni.2453

News and Views

Top

T. rex attacks the lysosome   pp10 - 12
Anna Katharina Simon and Andrea Ballabio
doi:10.1038/ni.2497
The mechanisms by which cells detect and fight foreign organisms is crucial for the host defense against infection. The sensing of cytosolic DNA is pivotal in this process, is kept in check by the exonuclease Trex1 and has been linked to lysosomal biogenesis via the transcription factor TFEB in an interferon-independent manner.

See also: Article by Hasan et al.

Just say NO to NLRP3   pp12 - 14
Manira Rayamajhi and Edward A Miao
doi:10.1038/ni.2493
Feedback inhibition by interferon-γ blocks the NLRP3 inflammasome by triggering inducible nitric oxide synthase (iNOS), and the resulting nitric oxide (NO) thio-nitrosylates NLRP3, shutting it down. This prevents excessive immunopathology during chronic infection with Mycobacterium tuberculosis.

See also: Article by Mishra et al.

Learning in motion: pericytes instruct migrating innate leukocytes   pp14 - 15
Ronen Alon and Sussan Nourshargh
doi:10.1038/ni.2489
During sterile inflammation, emigrating leukocytes sequentially engage subsets of pericytes associated with blood vessels and acquire adhesive, migratory and survival signals.

See also: Article by Stark et al.

Act1-hsp90 heats up TH17 inflammation   pp16 - 17
Pawan Kumar and Jay K Kolls
doi:10.1038/ni.2498
Psoriasis is associated with the TH17 subset of helper T cells. Dysregulation of interleukin 17 (IL-17) signaling leads to enhanced TH17 differentiation, more production of IL-22 and IL-22-dependent skin inflammation.

See also: Article by Wang et al.

Immunology
JOBS of the week
Postdoctoral position in Immunology and Immunotherapy
Inserm (French Institute of Health and Medical Research)
Postdoctoral Fellowship in Microbiology / Immunology
Prof Kristian Riesbeck
Microbiology / Virology Director Level Positions - Center for Immunology and Infectious Disease
SRI International, Biosciences Division
Manager outsourcing clinical immunology
Crucell Holland B.V.
Postdoc Position in Immunology
Novartis
More Science jobs from
Immunology
EVENT
5th ImmunoTherapeutics & ImmunoMonitoring
31st Jan - 1st Feb 2013
San Diego, US
More science events from

Research Highlights

Top

Viral infection: the clot thickens | Mimicking nickel allergy | It takes two | Activation by calcium | Building enhancers | Plasma-cell survival


Review

Top

STING and the innate immune response to nucleic acids in the cytosol   pp19 - 26
Dara L Burdette and Russell E Vance
doi:10.1038/ni.2491

Articles

Top

ARIH2 is essential for embryogenesis, and its hematopoietic deficiency causes lethal activation of the immune system   pp27 - 33
Amy E Lin, Gregor Ebert, Yongkai Ow, Simon P Preston, Jesse G Toe, James P Cooney, Hamish W Scott, Masato Sasaki, Samuel D Saibil, Dilan Dissanayake, Raymond H Kim, Andrew Wakeham, Annick You-Ten, Arda Shahinian, Gordon Duncan, Jennifer Silvester, Pamela S Ohashi, Tak W Mak and Marc Pellegrini
doi:10.1038/ni.2478
ARIH2 is a RING-between-RING E3 ligase. Pellegrini and colleagues show that ARIH2 is needed to limit excessive NF-κB signaling in DCs. Loss of ARIH2 is associated with embryonic death due to excessive inflammatory responses.

Neutrophil infiltration during inflammation is regulated by PILRα via modulation of integrin activation   pp34 - 40
Jing Wang, Ikuo Shiratori, Junji Uehori, Masahito Ikawa and Hisashi Arase
doi:10.1038/ni.2456
Modulation of integrin activation can contribute to regulation of inflammation. Arase and colleagues demonstrate that PILRα, an ITIM-containing inhibitory receptor, negatively regulates integrin activation and neutrophil infiltration during inflammation.

Capillary and arteriolar pericytes attract innate leukocytes exiting through venules and 'instruct' them with pattern-recognition and motility programs   pp41 - 51
Konstantin Stark, Annekathrin Eckart, Selgai Haidari, Anca Tirniceriu, Michael Lorenz, Marie-Luise von Brühl, Florian Gärtner, Alexander Georg Khandoga, Kyle R Legate, Robert Pless, Ingrid Hepper, Kirsten Lauber, Barbara Walzog and Steffen Massberg
doi:10.1038/ni.2477
The signals involved in coordinating the navigation of myeloid cells in tissues are incompletely understood. Massberg and colleagues show that NG2+ pericytes control the pattern and efficacy of interstitial leukocyte migration.

See also: News and Views by Alon & Nourshargh

Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome-dependent processing of IL-1β   pp52 - 60
Bibhuti B Mishra, Vijay A K Rathinam, Gregory W Martens, Amanda J Martinot, Hardy Kornfeld, Katherine A Fitzgerald and Christopher M Sassetti
doi:10.1038/ni.2474
Chronic infections can result in harmful production of the proinflammatory cytokine IL-1 generated via the NLRP3 inflammasome. Sassetti et al. demonstrate that IL-1 activated by Mycobacteria results in nitrosylation and consequent regulation of the NLRP3 inflammasome.

See also: News and Views by Rayamajhi & Miao

Trex1 regulates lysosomal biogenesis and interferon-independent activation of antiviral genes   pp61 - 71
Maroof Hasan, James Koch, Dinesh Rakheja, Asit K Pattnaik, James Brugarolas, Igor Dozmorov, Beth Levine, Edward K Wakeland, Min Ae Lee-Kirsch and Nan Yan
doi:10.1038/ni.2475
Trex1 is a cytosolic exonuclease that limits sensing of intracellular DNA. Yan and colleagues show that Trex1 deficiency spontaneously heightens adaptor STING-dependent proinflammatory responses via a pathway involving regulation of lysosomal biogenesis.

See also: News and Views by Simon & Ballabio

The psoriasis-associated D10N variant of the adaptor Act1 with impaired regulation by the molecular chaperone hsp90   pp72 - 81
Chenhui Wang, Ling Wu, Katarzyna Bulek, Bradley N Martin, Jarod A Zepp, Zizhen Kang, Caini Liu, Tomasz Herjan, Saurav Misra, Julie A Carman, Ji Gao, Ashok Dongre, Shujie Han, Kevin D Bunting, Jennifer S Ko, Hui Xiao, Vijay K Kuchroo, Wenjun Ouyang and Xiaoxia Li
doi:10.1038/ni.2479
Psoriasis is associated with heightened TH17 responses. Li and colleagues show that the IL-17R signaling adaptor Act1 requires the chaperone protein hsp90. Defective signaling leads to exuberant IL-22 production and enhanced disease.

See also: News and Views by Kumar & Kolls

Conformational states of the kinase Lck regulate clustering in early T cell signaling   pp82 - 89
Jérémie Rossy, Dylan M Owen, David J Williamson, Zhengmin Yang and Katharina Gaus
doi:10.1038/ni.2488
Gaus and colleagues show that the conformational states of the tyrosine kinase Lck intrinsically control its distribution and clustering at the plasma membrane.

Resource

Top

Shared and distinct transcriptional programs underlie the hybrid nature of iNKT cells   pp90 - 99
Nadia R Cohen, Patrick J Brennan, Tal Shay, Gerald F Watts, Manfred Brigl, Joonsoo Kang, Michael B Brenner and ImmGen Project Consortium
doi:10.1038/ni.2490
Using the Immunological Genome compendium, Brenner and colleagues shed light on the transcriptional programs that operate during the course of iNKT cell development and in peripheral CD4+ and CD4- iNKT cell subsets.

Top
 
Advertisement
Clinical & Translational Immunology (CTI)
Now Live - a new open access online-only journal publishing the latest and most exciting advances in biomedical research for scientists and physicians.

CTI promises the following benefits to all authors
- Wide exposure
- Quality peer-review and fast publication
- Research Summaries maximize the reach of your work

Discover more about CTI
 
nature events
Natureevents is a fully searchable, multi-disciplinary database designed to maximise exposure for events organisers. The contents of the Natureevents Directory are now live. The digital version is available here.
Find the latest scientific conferences, courses, meetings and symposia on natureevents.com. For event advertising opportunities across the Nature Publishing Group portfolio please contact natureevents@nature.com
More Nature Events

You have been sent this Table of Contents Alert because you have opted in to receive it. You can change or discontinue your e-mail alerts at any time, by modifying your preferences on your nature.com account at: www.nature.com/myaccount
(You will need to log in to be recognised as a nature.com registrant)

For further technical assistance, please contact our registration department

For print subscription enquiries, please contact our subscription department

For other enquiries, please contact our customer feedback department

Nature Publishing Group | 75 Varick Street, 9th Floor | New York | NY 10013-1917 | USA

Nature Publishing Group's worldwide offices:
London - Paris - Munich - New Delhi - Tokyo - Melbourne
San Diego - San Francisco - Washington - New York - Boston

Macmillan Publishers Limited is a company incorporated in England and Wales under company number 785998 and whose registered office is located at Brunel Road, Houndmills, Basingstoke, Hampshire RG21 6XS.

© 2013 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.

nature publishing group

No comments: