Nature Search

GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

An analysis of 24,202 critical cases of COVID-19 identifies potentially druggable targets in inflammatory signalling (JAK1), monocyte–macrophage activation and endothelial permeability (PDE4A), immunometabolism (SLC2A5 and AK5), and host factors required for viral entry and replication (TMPRSS2 and RAB2A).

Erola Pairo-Castineira
Konrad Rawlik
J. Kenneth Baillie
ResearchOpen Access17 May 2023
Nature

Volume: 617, P: 764-768
Mapping the human genetic architecture of COVID-19

A global network of researchers was formed to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity; this paper reports 13 genome-wide significant loci and potentially actionable mechanisms in response to infection.

Mari E. K. Niemi
Juha Karjalainen
Chloe Donohue
ResearchOpen Access08 Jul 2021
Nature

Volume: 600, P: 472-477
Whole-genome sequencing reveals host factors underlying critical COVID-19

Whole-genome sequencing, transcriptome-wide association and fine-mapping analyses in over 7,000 individuals with critical COVID-19 are used to identify 16 independent variants that are associated with severe illness in COVID-19.

Athanasios Kousathanas
Erola Pairo-Castineira
J. Kenneth Baillie
ResearchOpen Access07 Mar 2022
Nature

Volume: 607, P: 97-103
Calcium nanoparticles target and activate T cells to enhance anti-tumor function

Calcium signalling is an essential feature of T cell activation. Here authors employ CaCO₃ nanoparticles to facilitate the expansion and cytotoxic function of therapeutic T cells via enhanced intracellular release of calcium.

Wei Yang
Zhizi Feng
Jin Xie
ResearchOpen Access21 Nov 2024
Nature Communications

Volume: 15, P: 1-15
A second update on mapping the human genetic architecture of COVID-19

Masahiro Kanai
Shea J. Andrews
Matthew Solomonson
ResearchOpen Access06 Sept 2023
Nature

Volume: 621, P: E7-E26
Genetic mechanisms of critical illness in COVID-19

A genome-wide association study of critically ill patients with COVID-19 identifies genetic signals that relate to important host antiviral defence mechanisms and mediators of inflammatory organ damage that may be targeted by repurposing drug treatments.

Erola Pairo-Castineira
Sara Clohisey
J. Kenneth Baillie
Research11 Dec 2020
Nature

Volume: 591, P: 92-98
Author Correction: GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Erola Pairo-Castineira
Konrad Rawlik
J. Kenneth Baillie
Amendments and CorrectionsOpen Access11 Jul 2023
Nature

Volume: 619, P: E61
Interleukin-22: a sheep in wolf's clothing

Interleukin-22, a component of the immune system most studied for its role in autoimmunity, has a more beneficial side. Two studies show how this cytokine fights off microbes in the mucosa of the lung and gut (pages 275–281 and 282–289).

Arian Laurence
John J O'Shea
Wendy T Watford
News & Views01 Mar 2008
Nature Medicine

Volume: 14, P: 247-249
The immunity-related GTPase Irgm1 promotes the expansion of activated CD4⁺ T cell populations by preventing interferon-γ-induced cell death

Interferon-γ (IFN-γ) is toxic to cells, yet IFN-γ-producing cells survive. Feng and colleagues show that expression of the GTPase Irgm1 in these cells confers protection against IFN-γ toxicity.

Carl G Feng
Lixin Zheng
Alan Sher
Research21 Sept 2008
Nature Immunology

Volume: 9, P: 1279-1287
Genomic reconstruction of the SARS-CoV-2 epidemic in England

A study of the evolution of the SARS-CoV-2 virus in England between September 2020 and June 2021 finds that interventions capable of containing previous variants were insufficient to stop the more transmissible Alpha and Delta variants.

Harald S. Vöhringer
Theo Sanderson
Moritz Gerstung
ResearchOpen Access14 Oct 2021
Nature

Volume: 600, P: 506-511
Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

Openshaw and colleagues find myeloid inflammation and complement activation signatures in patients with long COVID who were previously hospitalized.

Felicity Liew
Claudia Efstathiou
J. Eunice Zhang
ResearchOpen Access08 Apr 2024
Nature Immunology

Volume: 25, P: 607-621
SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

The Omicron variant evades vaccine-induced neutralization but also fails to form syncytia, shows reduced replication in human lung cells and preferentially uses a TMPRSS2-independent cell entry pathway, which may contribute to enhanced replication in cells of the upper airway. Altered fusion and cell entry characteristics are linked to distinct regions of the Omicron spike protein.

Brian J. Willett
Joe Grove
Emma C. Thomson
ResearchOpen Access07 Jul 2022
Nature Microbiology

Volume: 7, P: 1161-1179
T-cell-expressed proprotein convertase furin is essential for maintenance of peripheral immune tolerance

Conditional knockout of the protease furin in CD4⁺ T cells is shown to result in impaired peripheral tolerance and autoimmune disease. Furin deficiency compromises TGF-β release and T_reg function, and is associated with inherently more aggressive effector T cells.

Marko Pesu
Wendy T. Watford
John J. O’Shea
Research13 Aug 2008
Nature

Volume: 455, P: 246-250
A case of mistaken identity

The interleukin-12 protein has been implicated in autoimmunity, but one complication is that it shares a subunit with a related protein. New work looks at the contribution of these proteins to autoimmunity in mice.

Wendy T. Watford
John J. O'Shea
News & Views13 Feb 2003
Nature

Volume: 421, P: 706-707
Generation of pathogenic T_H17 cells in the absence of TGF-β signalling

CD4⁺ T cells that selectively produce interleukin (IL)-17 (T_H17 cells) are essential for host defence and autoimmunity. It has been thought that IL-6 and transforming growth factor (TGF)-β1 are the factors responsible for initiating the specification of T_H17 cells. Here, however, it is shown that T_H17 differentiation can occur in the absence of TGF-β signalling. IL-6, IL-23 and IL-1β effectively induced IL-17 production in naive precursors. These data reveal an alternative mode for T_H17 differentiation and the importance of IL-23.

Kamran Ghoreschi
Arian Laurence
John J. O’Shea
Research20 Oct 2010
Nature

Volume: 467, P: 967-971
Inhibition of glycogen synthase kinase-3 by BTA-EG₄ reduces tau abnormalities in an organotypic brain slice culture model of Alzheimer’s disease

Cara L. Croft
Ksenia Kurbatskaya
Wendy Noble
ResearchOpen Access07 Aug 2017
Scientific Reports

Volume: 7, P: 1-11
A peek at PIAS

Members of the PIAS family can negatively regulate the cytokine-activated Jak-STAT pathway in vitro. One member of this family, PIAS1, is a nonredundant and physiologic regulator of certain STAT1-dependent interferon-induced genes.

John J O'Shea
Wendy Watford
News & Views01 Sept 2004
Nature Immunology

Volume: 5, P: 875-876
Morphine activation of mu opioid receptors causes disinhibition of neurons in the ventral tegmental area mediated by β-arrestin2 and c-Src

Fiona A. Bull
Daniel T. Baptista-Hon
Tim G. Hales
ResearchOpen Access30 Aug 2017
Scientific Reports

Volume: 7, P: 1-11
CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Chromodomain Helicase DNA-binding (CHD) proteins have been implicated in neurodevelopmental processes. Here, the authors identify missense variants in CHD3 that disturb its chromatin remodeling activities and cause a neurodevelopmental disorder with macrocephaly and speech and language impairment.

Lot Snijders Blok
Justine Rousseau
Philippe M. Campeau
ResearchOpen Access05 Nov 2018
Nature Communications

Volume: 9, P: 1-12
Prevalence and architecture of de novo mutations in developmental disorders

Whole-exome analysis of individuals with developmental disorders shows that de novo mutations can equally cause loss or altered protein function, but that most mutations causing altered protein function have not yet been described.

Jeremy F. McRae
Stephen Clayton
Matthew E. Hurles
Research25 Jan 2017
Nature

Volume: 542, P: 433-438
Publisher Correction: Genomic reconstruction of the SARS CoV-2 epidemic in England

Harald S. Vöhringer
Theo Sanderson
Moritz Gerstung
Amendments and CorrectionsOpen Access07 Jun 2022
Nature

Volume: 606, P: E18
Membrane association and release of wild-type and pathological tau from organotypic brain slice cultures

Cara L Croft
Matthew A Wade
Wendy Noble
ResearchOpen Access16 Mar 2017
Cell Death & Disease

Volume: 8, P: e2671
Acute irradiation induces a senescence-like chromatin structure in mammalian oocytes

Super-resolution imaging and RNA clock analyses show that exposure of mouse oocytes to ionizing radiation compromises chromatin organization and dramatically accelerates biological aging.

Claudia Baumann
Xiangyu Zhang
Rabindranath De La Fuente
ResearchOpen Access12 Dec 2023
Communications Biology

Volume: 6, P: 1-16
A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3

Ian PM Tomlinson
Emily Webb
Richard S Houlston
Research30 Mar 2008
Nature Genetics

Volume: 40, P: 623-630
Publisher Correction: SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

Brian J. Willett
Joe Grove
Emma C. Thomson
Amendments and CorrectionsOpen Access16 Sept 2022
Nature Microbiology

Volume: 7, P: 1709
COVID-19 due to the B.1.617.2 (Delta) variant compared to B.1.1.7 (Alpha) variant of SARS-CoV-2: a prospective observational cohort study

Kerstin Kläser
Erika Molteni
Emma L. Duncan
ResearchOpen Access28 Jun 2022
Scientific Reports

Volume: 12, P: 1-17
Genomic epidemiology of SARS-CoV-2 in a university outbreak setting and implications for public health planning

Sema Nickbakhsh
Joseph Hughes
Alison Smith-Palmer
ResearchOpen Access19 Jul 2022
Scientific Reports

Volume: 12, P: 1-17
Breast cancer management pathways during the COVID-19 pandemic: outcomes from the UK ‘Alert Level 4’ phase of the B-MaP-C study

Rajiv V. Dave
Baek Kim
Zaid Al-Ishaq
ResearchOpen Access25 Mar 2021
British Journal of Cancer

Volume: 124, P: 1785-1794
Author Correction: CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Lot Snijders Blok
Justine Rousseau
Philippe M. Campeau
Amendments and CorrectionsOpen Access15 Feb 2019
Nature Communications

Volume: 10, P: 1-4
Author Correction: CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Lot Snijders Blok
Justine Rousseau
Philippe M. Campeau
Amendments and CorrectionsOpen Access02 May 2019
Nature Communications

Volume: 10, P: 1-4
Telomerecat: A ploidy-agnostic method for estimating telomere length from whole genome sequencing data

James H. R. Farmery
Mike L. Smith
Andy G. Lynch
ResearchOpen Access22 Jan 2018
Scientific Reports

Volume: 8, P: 1-17
Publisher Correction: Telomerecat: A ploidy-agnostic method for estimating telomere length from whole genome sequencing data

James H. R. Farmery
Mike L. Smith
Andy G. Lynch
Amendments and CorrectionsOpen Access03 Sept 2018
Scientific Reports

Volume: 8, P: 1-4

Search

GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Mapping the human genetic architecture of COVID-19

Whole-genome sequencing reveals host factors underlying critical COVID-19

Calcium nanoparticles target and activate T cells to enhance anti-tumor function

A second update on mapping the human genetic architecture of COVID-19

Genetic mechanisms of critical illness in COVID-19

Author Correction: GWAS and meta-analysis identifies 49 genetic variants underlying critical COVID-19

Interleukin-22: a sheep in wolf's clothing

The immunity-related GTPase Irgm1 promotes the expansion of activated CD4⁺ T cell populations by preventing interferon-γ-induced cell death

Genomic reconstruction of the SARS-CoV-2 epidemic in England

Large-scale phenotyping of patients with long COVID post-hospitalization reveals mechanistic subtypes of disease

SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

T-cell-expressed proprotein convertase furin is essential for maintenance of peripheral immune tolerance

A case of mistaken identity

Generation of pathogenic T_H17 cells in the absence of TGF-β signalling

Inhibition of glycogen synthase kinase-3 by BTA-EG₄ reduces tau abnormalities in an organotypic brain slice culture model of Alzheimer’s disease

A peek at PIAS

Morphine activation of mu opioid receptors causes disinhibition of neurons in the ventral tegmental area mediated by β-arrestin2 and c-Src

CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Prevalence and architecture of de novo mutations in developmental disorders

Publisher Correction: Genomic reconstruction of the SARS CoV-2 epidemic in England

Membrane association and release of wild-type and pathological tau from organotypic brain slice cultures

Acute irradiation induces a senescence-like chromatin structure in mammalian oocytes

A genome-wide association study identifies colorectal cancer susceptibility loci on chromosomes 10p14 and 8q23.3

Publisher Correction: SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

COVID-19 due to the B.1.617.2 (Delta) variant compared to B.1.1.7 (Alpha) variant of SARS-CoV-2: a prospective observational cohort study

Genomic epidemiology of SARS-CoV-2 in a university outbreak setting and implications for public health planning

Breast cancer management pathways during the COVID-19 pandemic: outcomes from the UK ‘Alert Level 4’ phase of the B-MaP-C study

Author Correction: CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Author Correction: CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language

Telomerecat: A ploidy-agnostic method for estimating telomere length from whole genome sequencing data

Publisher Correction: Telomerecat: A ploidy-agnostic method for estimating telomere length from whole genome sequencing data

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