Tuesday, June 20, 2017

Nature Immunology Contents: July 2017 Volume 18 pp 707 - 823

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Nature Immunology


July 2017 Volume 18, Issue 7

News and Views
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Julius Youngner 1920-2017   p707
Vincent Racaniello

News and Views


Polymorphisms in IFIH1: the good and the bad   pp708 - 709
Erika Della Mina, Mathieu P Rodero and Yanick J Crow
A study of polymorphisms in the sensor IFIH1 exposes the evolutionary trade-off between a robust antiviral type I interferon response and the risk of interferon-mediated inflammation.

See also: Article by Gorman et al.

A Hippo in the Fox(p3) house   pp709 - 711
Mandy J McGeachy
The Hippo signaling pathway regulates cellular proliferation and survival during tissue growth and cancer. In CD4+ T cells, members of the Hippo family modulate autoimmune inflammation by altering interactions between the transcription factors Foxp3 and RORγt; this reveals an unexpected non-canonical role for Hippo in adaptive immunity.

See also: Article by Geng et al.

Atypical matters in myeloid differentiation   pp711 - 712
Massimo Locati, Alberto Mantovani and Raffaella Bonecchi
Chemokines are important components of the hematopoietic niche. The atypical chemokine receptor 1 (ACKR1), expressed on erythrocyte precursors, regulates myeloid differentiation.

See also: Article by Duchene et al.

A rheostat tuning thymic selection   pp713 - 714
Gerald P Morris and Stephen M Hedrick
Thymocytes must undergo positive selection to survive and differentiate. This process is regulated by the TCR-sensitive protein CHMPS by preventing Bcl2 oxidation and degradation.

See also: Article by Adoro et al.

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Research Highlights


Learning during inflammation | Highly localized memory | Tissue-specific amplifiers | Regulating hair growth | IL-22 in Peyer's patches | Epigenetic changes in TILs



The multiple pathways to autoimmunity   pp716 - 724
Argyrios N Theofilopoulos, Dwight H Kono and Roberto Baccala
Autoimmunity can arise when tolerance mechanisms break down. Theofilopoulos and colleagues review how loss of peripheral tolerance, often driven by innate nucleic-acid sensors, leads to the activation of autoreactive lymphocytes that underlie many autoimmune diseases.

Systems immunology: just getting started   pp725 - 732
Mark M Davis, Cristina M Tato and David Furman
Davis and colleagues review systems-biology approaches in immunology as a powerful means of understanding the immune system as a whole.



YAP antagonizes innate antiviral immunity and is targeted for lysosomal degradation through IKK¤Á-mediated phosphorylation   pp733 - 743
Shuai Wang, Feng Xie, Feng Chu, Zhengkui Zhang, Bing Yang et al.
Intracellular detection of viral invasion triggers activation of the transcription factor IRF3 and antiviral interferon production. Fangfang Zhou and colleagues report that the transcription regulator YAP in the host restrains this process by preventing inadvertent spontaneous dimerization of IRF3 and its translocation to the nucleus.

The A946T variant of the RNA sensor IFIH1 mediates an interferon program that limits viral infection but increases the risk for autoimmunity   pp744 - 752
Jacquelyn A Gorman, Christian Hundhausen, John S Errett, Amy E Stone, Eric J Allenspach et al.
Single-nucleotide polymorphisms in the gene encoding the cytosolic viral sensor IFIH1 are linked to a variety of autoimmune diseases. Rawlings and colleagues demonstrate that one such common polymorphism results in IFIH1 with more-potent activation and can act synergistically with other genetic backgrounds to manifest autoimmune disease.

See also: News and Views by Mina et al.

Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis   pp753 - 761
Johan Duchene, Igor Novitzky-Basso, Aude Thiriot, Maria Casanova-Acebes, Mariaelvy Bianchini et al.
Genetic polymorphisms affect expression of the atypical chemokine receptor ACKR1 (Duffy) on nucleated erythrocyte precursors. Rot and colleagues show that loss of its expression alters hematopoiesis, yielding a distinct neutrophil population that rapidly exits the bloodstream to give an apparent 'neutropenia' phenotype.

See also: News and Views by Locati et al.

Dendritic cells enter lymph vessels by hyaluronan-mediated docking to the endothelial receptor LYVE-1   pp762 - 770
Louise A Johnson, Suneale Banerji, William Lawrance, Uzi Gileadi, Gennaro Prota et al.
Jackson and colleagues show that dendritic cells transit to the lumen of lymphatic vessels through hyaluronan-mediated interactions with the endothelial receptor LYVE-1.

CD8αα intraepithelial lymphocytes arise from two main thymic precursors   pp771 - 779
Roland Ruscher, Rebecca L Kummer, You Jeong Lee, Stephen C Jameson and Kristin A Hogquist
TCRβ+CD8αα+ intraepithelial lymphocytes arise from CD4-CD8-CD5+ thymic cells, but the exact precursor source has been not been established. Hogquist and colleagues identify two distinct thymic populations that both give rise mainly to gut-homing intraepithelial lymphocytes.

Post-translational control of T cell development by the ESCRT protein CHMP5   pp780 - 790
Stanley Adoro, Kwang Hwan Park, Sarah E Bettigole, Raphael Lis, Hee Rae Shin et al.
Thymocytes must undergo positive selection to survive and emigrate to the periphery as mature T cells. Glimcher and colleagues identify CHMP5 as a TCR-sensitive regulator of positive selection that acts by preventing oxidation and degradation of the pro-survival protein Bcl-2.

See also: News and Views by Morris & Hedrick

The microRNA miR-31 inhibits CD8+ T cell function in chronic viral infection   pp791 - 799
Howell F Moffett, Adam N R Cartwright, Hye-Jung Kim, Jernej Godec, Jason Pyrdol et al.
Wucherpfennig and colleagues show that the microRNA miR-31 increases the sensitivity of T cells to type I interferons, which interferes with effector T cell function during chronic infection.

The transcriptional coactivator TAZ regulates reciprocal differentiation of TH17 cells and Treg cells   pp800 - 812
Jing Geng, Shujuan Yu, Hao Zhao, Xiufeng Sun, Xun Li et al.
Hippo signaling controls cell and tissue growth. Geng et al. show that Hippo signaling is required for TH17 cell differentiation but inhibits Treg cell differentiation.

See also: News and Views by McGeachy

BACH2 immunodeficiency illustrates an association between super-enhancers and haploinsufficiency   pp813 - 823
Behdad Afzali, Juha Grönholm, Jana Vandrovcova, Charlotte O'Brien, Hong-Wei Sun et al.
BACH2 is required for lymphocyte differentiation. Afzali et al. describe mutations that cause BACH2 disruption, immunodeficiency and autoinflammatory disease via haploinsufficiency, a mechanism shared by other super-enhancer-regulated genes.

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