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2013/01/18

Nature Immunology Contents: February 2013 Volume 14 pp 101 - 185

Nature Immunology
TABLE OF CONTENTS

February 2013 Volume 14, Issue 2

Meeting Report
Commentary
News and Views
Research Highlights
Review
Articles
Resource



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Meeting Report

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Understanding the microbiota in the midst of Renaissance architecture and olive groves   pp101 - 105
Francisco Guarner, Lora V Hooper and Gabriel Núñez
doi:10.1038/ni.2512

Commentary

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Personalizing medicine for autoimmune and inflammatory diseases   pp106 - 109
Andrew C Chan and Timothy W Behrens
doi:10.1038/ni.2473

News and Views

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A complement a day keeps the Fox(p3) away   pp110 - 112
Gaelle Le Friec, Jörg Köhl and Claudia Kemper
doi:10.1038/ni.2515
Signaling via the complement factors C3a and C5a regulates effector T cell responses. Evidence now links the absence of local complement activation with a default pathway that leads to the polarization of Foxp3+ regulatory T cells.

See also: Article by Strainic et al.

Too much of a good thing   pp112 - 114
Atsushi Onodera, Damon John Tumes and Toshinori Nakayama
doi:10.1038/ni.2510
Maintenance of the peripheral naive CD8+ T cell pool depends on T cell antigen receptor (TCR) signals and interleukin 7 (IL-7). TCR signaling limits the duration of IL-7 signals to avoid an interferon-γ-mediated mechanism of apoptotic death of naive CD8+ T cells.

See also: Article by Kimura et al.

Paneth cells: targets of friendly fire   pp114 - 116
Stephen J McSorley and Charles L Bevins
doi:10.1038/ni.2519
Severe intestinal pathology associated with infection with Toxoplasma gondii is a result of the loss of Paneth cells, an unexpected side effect of the secretion of IFN-γ by protective CD4+ T cells in the intestinal mucosa.

See also: Article by Raetz et al.

Noncanonical NFATc1 activation in DN thymocytes   pp116 - 117
Fernando Macian
doi:10.1038/ni.2522
Double-negative (DN) thymocytes depend on interleukin 7 (IL-7) for survival. In DN2 and DN3 cells, a new role has now been identified for signaling via the IL-7 receptor and the kinase Jak3 that leads to noncanonical activation of the transcription factor NFATc1 and upregulation of expression of the antiapoptotic protein Bcl-2.

See also: Article by Patra et al.

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Research Highlights

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DC defects in HIV-1 | Maturing pDCs | Cereals activate TLR4 | Nonprofessional phagocytes | Macrophage Jnk | NLRP3 ubiquitination


Review

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Innate B cell helpers reveal novel types of antibody responses   pp119 - 126
Carola G Vinuesa and Pheh-Ping Chang
doi:10.1038/ni.2511

Articles

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An alternative NFAT-activation pathway mediated by IL-7 is critical for early thymocyte development   pp127 - 135
Amiya K Patra, Andris Avots, René P Zahedi, Thomas Schuler, Albert Sickmann, Ursula Bommhardt and Edgar Serfling
doi:10.1038/ni.2507
Interleukin 7 (IL-7) signaling is essential during early lymphocyte development. Patra and colleagues identify a distinct IL-7-kinase Jak3-dependent pathway that activates the transcription factor NFATc1 in DN1 thymocytes to promote their survival.

See also: News and Views by Macian

Parasite-induced TH1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells   pp136 - 142
Megan Raetz, Sun-hee Hwang, Cara L Wilhelm, Donna Kirkland, Alicia Benson, Carolyn R Sturge, Julie Mirpuri, Shipra Vaishnava, Baidong Hou, Anthony L DeFranco, Christopher J Gilpin, Lora V Hooper and Felix Yarovinsky
doi:10.1038/ni.2508
Immune responses can cause immunopathology. Yarovinsky and colleagues show that IFN-γ induced by T cell-intrinsic TLR signaling in CD4+ TH1 cells during Toxoplasma gondii infection causes dysbiosis and loss of Paneth cells.

See also: News and Views by McSorley & Bevins

IL-7 signaling must be intermittent, not continuous, during CD8+ T cell homeostasis to promote cell survival instead of cell death   pp143 - 151
Motoko Y Kimura, Leonid A Pobezinsky, Terry I Guinter, Julien Thomas, Anthony Adams, Jung-Hyun Park, Xuguang Tai and Alfred Singer
doi:10.1038/ni.2494
Why signaling via both the receptor for interleukin 7 (IL-7R) and the T cell antigen receptor (TCR) is required for T cell homeostasis has been unclear. Singer and colleagues show that engagement of the TCR interrupts IL-7R signals to prevent a mechanism of cytokine-induced cell death.

See also: News and Views by Onodera et al.

The receptor PD-1 controls follicular regulatory T cells in the lymph nodes and blood   pp152 - 161
Peter T Sage, Loise M Francisco, Christopher V Carman and Arlene H Sharpe
doi:10.1038/ni.2496
Follicular regulatory T cells control humoral immune responses, but how these cells are in turn controlled has been unclear. Sharpe and colleagues demonstrate that signaling via PD-1 regulates number and function of these cells.

Absence of signaling into CD4+ cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3+ regulatory T cells   pp162 - 171
Michael G Strainic, Ethan M Shevach, Fengqi An, Feng Lin and M Edward Medof
doi:10.1038/ni.2499
Complement provides costimulatory signals to T cells. Medof and colleagues demonstrate that an absence of complement signaling in naive T cells generates an autoinductive loop to drive induced regulatory T cells.

See also: News and Views by Le Friec et al.

The E3 ubiquitin ligase TRIM21 negatively regulates the innate immune response to intracellular double-stranded DNA   pp172 - 178
Zhiqiang Zhang, Musheng Bao, Ning Lu, Leiyun Weng, Bin Yuan and Yong-Jun Liu
doi:10.1038/ni.2492
The intracellular sensor DDX41 is important for generating innate responses to DNA viruses. Liu et al. demonstrate that the ubiquitin ligase TRIM21 degrades and thereby regulates DDX41-dependent responses.

Resource

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Identification of regulators of the innate immune response to cytosolic DNA and retroviral infection by an integrative approach   pp179 - 185
Mark N Lee, Matthew Roy, Shao-En Ong, Philipp Mertins, Alexandra-Chloé Villani, Weibo Li, Farokh Dotiwala, Jayita Sen, John G Doench, Megan H Orzalli, Igor Kramnik, David M Knipe, Judy Lieberman, Steven A Carr and Nir Hacohen
doi:10.1038/ni.2509
Hacohen and colleagues use an integrative approach that combines quantitative proteomics, genomics and small molecule perturbations to identify new genes involved in DNA sensing and type I interferon production.

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