Tuesday, October 20, 2015

Nature Immunology Contents: November 2015 Volume 16 pp 1105 - 1203

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TABLE OF CONTENTS

November 2015 Volume 16, Issue 11

News and Views
Research Highlights
Review
Articles
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News and Views

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Reversed-polarity Treg cell TCRs provide a shock   pp1105 - 1107
Mark Peakman and Andrew K Sewell
doi:10.1038/ni.3289
Docking of T cell antigen receptors (TCRs) engaging complexes of peptide and major histocompatibility complex has shown the same diagonal orientation and polarity. A new study demonstrating that TCRs from regulatory T cells bind with reversed polarity challenges this dogma.

See also: Article by Beringer et al.

De-Mst-ifying microbicidal killing   pp1107 - 1108
Lynda M Stuart and Adam Lacy-Hulbert
doi:10.1038/ni.3291
Mitochondria can contribute to an increase in the amount of phagosomal reactive oxygen species and thereby promote the effective killing of bacteria. Study of mice deficient in Mst1 and Mst2 reveals a role for these kinases in recruiting mitochondria to phagosomes.

See also: Article by Geng et al.

MicroRNA miR-22 drives TH17 responses in emphysema   pp1109 - 1110
Guy G Brusselle and Ken R Bracke
doi:10.1038/ni.3295
The TH17 subset of helper T cells drives emphysema in smokers, but how these cells are elicited remains unknown. A study now links the microRNA miR-22 and the histone deacetylase HDAC4 to regulation of the activation of antigen-presenting cells after exposure to smoke.

See also: Article by Lu et al.

Drosha cuts the tethers of myelopoiesis   pp1110 - 1112
Annemarthe G van der Veen, Pierre V Maillard and Caetano Reis e Sousa
doi:10.1038/ni.3297
The RNA endonuclease Drosha is required for myelopoiesis by its direct cleavage of stem-loop structures in mRNAs encoding Myl9 and Todr1.

See also: Article by Johanson et al.

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Research Highlights

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Melatonin zaps TH17 | SLE links to Alu elements | cGAS ramps up autoinflammatory disease | Don't eat me, activate me | Aging neutrophils | Preserving intestinal stem cells

Review

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The burgeoning family of unconventional T cells   pp1114 - 1123
Dale I Godfrey, Adam P Uldrich, James McCluskey, Jamie Rossjohn and D Branch Moody
doi:10.1038/ni.3298
While most studies of T lymphocytes have focused on peptide-MHC-reactive T cells, many other types of T cells do not fit this paradigm. Here Godfrey et al. review the immunology of such unconventional T cells.

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Articles

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Runx3 specifies lineage commitment of innate lymphoid cells   pp1124 - 1133
Takashi Ebihara, Christina Song, Stacy H Ryu, Beatrice Plougastel-Douglas, Liping Yang et al.
doi:10.1038/ni.3272
The transcriptional control of lineage commitment to various ILC subsets is incompletely understood. Yokoyama and colleagues show that Runx3 is essential for the normal development of ILC1 and ILC3 cells but not ILC2 cells.

Drosha controls dendritic cell development by cleaving messenger RNAs encoding inhibitors of myelopoiesis   pp1134 - 1141
Timothy M Johanson, Ashleigh A Keown, Marek Cmero, Janet H C Yeo, Amit Kumar et al.
doi:10.1038/ni.3293
The enzyme Drosha is associated with the biogenesis of microRNA. Chong and colleagues identify a non- microRNA function for Drosha in dendritic cell development.

See also: News and Views by van der Veen et al.

Kinases Mst1 and Mst2 positively regulate phagocytic induction of reactive oxygen species and bactericidal activity   pp1142 - 1152
Jing Geng, Xiufeng Sun, Ping Wang, Shihao Zhang, Xiaozhen Wang et al.
doi:10.1038/ni.3268
Mitochondria must be juxtaposed to phagosomes to supply reactive oxygen species for effective killing of microbes. Zhou and colleagues demonstrate that the kinases Mst1 and Mst2 are important for controlling this redistribution of mitochondria.

See also: News and Views by Stuart & Lacy-Hulbert

T cell receptor reversed polarity recognition of a self-antigen major histocompatibility complex   pp1153 - 1161
Dennis X Beringer, Fleur S Kleijwegt, Florian Wiede, Arno R van der Slik, Khai Lee Loh et al.
doi:10.1038/ni.3271
To date, structural analysis has demonstrated a highly consistent binding pattern of the TCR to the MHC molecule. Rossjohn and colleagues reveal the first structures of two human Treg cell TCRs and show that they bind with a reversed polarity to the MHC.

See also: News and Views by Peakman & Sewell

Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling   pp1162 - 1173
Louis-Marie Charbonnier, Sen Wang, Peter Georgiev, Esen Sefik and Talal A Chatila
doi:10.1038/ni.3288
Chatila and colleagues demonstrate a critical role for Notch canonical and non-canonical signaling in controlling peripheral Treg cell function.

Glycolysis controls the induction of human regulatory T cells by modulating the expression of FOXP3 exon 2 splicing variants   pp1174 - 1184
Veronica De Rosa, Mario Galgani, Antonio Porcellini, Alessandra Colamatteo, Marianna Santopaolo et al.
doi:10.1038/ni.3269
The metabolic requirements of T cells vary according to their functional state. Matarese and colleagues show that the most functionally active human regulatory T cells are highly glycolytic and that this directly controls expression of a distinct splice variant of the transcription factor Foxp3.

The microRNA miR-22 inhibits the histone deacetylase HDAC4 to promote TH17 cell-dependent emphysema   pp1185 - 1194
Wen Lu, Ran You, Xiaoyi Yuan, Tianshu Yang, Errol L G Samuel et al.
doi:10.1038/ni.3292
Smoking can lead to emphysema. Corry and colleagues show that smoke and carbon black particles induce the microRNA miR-22 as a mediator that suppresses expression of the histone deacetylase HDAC4 and thereby promotes a chronic TH17 cell-dependent inflammatory response.

See also: News and Views by Brusselle & Bracke

TCR-induced sumoylation of the kinase PKC-θ controls T cell synapse organization and T cell activation   pp1195 - 1203
Xu-Dong Wang, Yu Gong, Zhi-Long Chen, Bei-Ni Gong, Ji-Ji Xie et al.
doi:10.1038/ni.3259
Sumoylation regulates many cellular processes, but its role in TCR signaling remains unknown. Li and colleagues show that sumoylation of the kinase PKC-θ is required for the assembly of a mature immunological synapse.

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