Monday, February 27, 2017

Nature Reviews Immunology Contents March 2017 Volume 17 Number 3 pp 145-214

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Nature Reviews Immunology

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March 2017 Volume 17 Number 3
Nature Reviews Immunology cover
2015 2-year Impact Factor 39.416 Journal Metrics 2-year Median 31
In this issue
Research Highlights

Also this month
Article series:
Cell death and immunity
 Featured article:
Regulation of muscle growth and regeneration by the immune system
James G. Tidball

Recommend to library

Immunometabolism: Powering down leukaemia
p145 | doi:10.1038/nri.2017.17
B-lymphoid transcription factors can protect against leukaemic transformation by restricting glucose and energy usage in pre-B cells.


Infection: IL-22 controls iron scavenging
p146 | doi:10.1038/nri.2017.15
During systemic infection interleukin-22 can limit the availability of iron by promoting increased production of haem scavengers.


Mucosal immunology: Rationing AHR ligands
p146 | doi:10.1038/nri.2017.8
CYP1 enzymes expressed by intestinal epithelial cells metabolise AHR ligands in the gut to regulate intestinal immune responses.


Infectious disease: Hitching a ride with DCs
p147 | doi:10.1038/nri.2017.16
Pseudogenization of a single Salmonella effector protein gene facilitates pathogen hijacking of dendritic cells to spread systemically.


Macrophages: mTORC1 drives granulomas
p148 | doi:10.1038/nri.2017.14
MTORC1-dependent macrophage proliferation and glycolysis drive granuloma formation in sarcoidosis.


Fungal infection: JNK inhibitors boost antifungal immunity
p148 | doi:10.1038/nri.2017.18

Multi-dimensional control of clonal evolution

p149 | doi:10.1038/nri.2017.6
Michael McHeyzer-Williams describes a 1998 study by Avi Kupfer and colleagues that transformed the view of cognate T helper cell-B cell crosstalk.


Nature Reviews Immunology
JOBS of the week
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Ecole Polytechnique Fédérale de Lausanne (EPFL)
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The Hong Kong Polytechnic University
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Kleo Pharmaceuticals
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Erasmus MC
Bioinformatician on Immunology: Osaka, Japan
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Article series: Cell death and immunity
Programmed cell death as a defence against infection
Ine Jorgensen, Manira Rayamajhi & Edward A. Miao
p151 | doi:10.1038/nri.2016.147
This Review describes how different modes of cell death protect against bacterial and viral infections, and the complex signalling crosstalk between the different pathways during an infection.
Abstract | Full Text | PDF | Supplementary information

Regulation of muscle growth and regeneration by the immune system
James G. Tidball
p165 | doi:10.1038/nri.2016.150
Following muscle injury, changes in the stages of muscle growth coincide with changes in the phenotype and activation status of leukocytes that enter the site of muscle damage. As described in this Review, complex and coordinated crosstalk between immune cells and muscle cells determines the success or failure of muscle regeneration.
Abstract | Full Text | PDF

T cell responses in the central nervous system
Thomas Korn & Axel Kallies
p179 | doi:10.1038/nri.2016.144
This Review focuses on the protective and pathological roles of different T cell subsets in the central nervous system (CNS). The authors explain how effector, memory and regulatory T cell populations are primed and recruited to the CNS, and discuss the plasticity of these populations, particularly in the context of viral infection and autoimmunity.
Abstract | Full Text | PDF

Immunobiology of Ebola and Lassa virus infections
Joseph B. Prescott et al.
p195 | doi:10.1038/nri.2016.138
Severe haemorrhagic fever is a feature of infection with both Ebola and Lassa viruses, but differences in the immune responses induced by infection in each case may have important implications for the development of specific therapies and vaccines.
Abstract | Full Text | PDF | Supplementary information

Homeostasis-altering molecular processes as mechanisms of inflammasome activation
Adrian Liston & Seth L. Masters
p208 | doi:10.1038/nri.2016.151
Innate immune responses are triggered in response to the sensing of pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) by pattern recognition receptors (PRRs). An emerging idea is that inflammasome activation may also occur independently of PRR activation following a disturbance in cellular homeostasis. The authors explore this concept and the implications for chronic inflammatory disease in this Opinion article.
Abstract | Full Text | PDF

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