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James A. Nathan on Muck Rack

James A. Nathan

United Kingdom
As seen in: Fabulous, HuffPost, Nature, JSTOR Daily, PNAS, Science Magazine, BioRxiv, Foreign Affairs, Recruiter
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Author Correction: Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity | Nature Immunology

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By Manuel A. Sánchez-García, David Griffith, Tyler Morrison, Ananda S. Mirchandani, Simone Arienti, Xiang Xu, Alejandro J Brenes, Rebecca Dowey, Oliver Vick, Isla Petrie, Suzanne Green, Nina M Rzechorzek, Malcolm G Semple, J. Kenneth Baillie, Alfred A. R. Thompson, David Mole, Alex von Kriegsheim, Musa M. Mhlanga, James A. Nathan
| Nature Verified
Correction to: Nature Immunology https://doi.org/10.1038/s41590-025-02301-9, published online 28 October 2025. In the version of this article initially published, the surname of Musa M. Mhlanga was misspelled (Mhalanga) and is now amended in the HTML and PDF versions of the article.
Open in Who Shared View Duplicates (2) Issue with article?

Mitochondrial ABHD11 inhibition drives sterol metabolism to modulate T-cell effector function - Nature Communications

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By Chloe Moscrop, Iain A. Perry, Matthew D Hitchings, Simon Eastham, James Cronin, Douglas J. Veale, David Finlay Verified, Linda Sinclair, Benjamin Cravatt, Andrew Hogan, James A. Nathan, Ian R Humphreys, Johan Vande Voorde, Jeffrey McDonald, Gareth Jones, James Pearson Verified, Emma Vincent
| Nature Verified
Abstract α/β-hydrolase domain-containing protein 11 (ABHD11) is a mitochondrial hydrolase that maintains the catalytic function of α-ketoglutarate dehydrogenase (α-KGDH), and its expression in CD4 + T-cells has been linked to remission status in rheumatoid arthritis (RA). However, the importance of ABHD11 in regulating T-cell metabolism and function is yet to be explored. Here, we show that pharmacological inhibition of ABHD11 dampens cytokine production by human and mouse T-cells.
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Hypoxia induces histone clipping and H3K4me3 loss in neutrophil progenitors resulting in long-term impairment of neutrophil immunity - Nature Immunology

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By Manuel A. Sánchez-García, David Griffith, Tyler Morrison, Ananda S. Mirchandani, Simone Arienti, Xiang Xu, Alejandro J Brenes, Rebecca Dowey, Suzanne Green, Nina M Rzechorzek, Malcolm G Semple, J. Kenneth Baillie, Alfred A. R. Thompson, David Mole, Alex von Kriegsheim, James A. Nathan, Oliver Vick, Isla Petrie, Musa M. Mhalanga
| Nature Verified
Abstract The long-term impact of systemic hypoxia resulting from acute respiratory distress syndrome (ARDS) on the function of short-lived innate immune cells is unclear. We show that patients 3–6 months after recovering from ARDS have persistently impaired circulating neutrophil effector functions and an increased susceptibility to secondary infections. These defects are linked to a widespread loss of the activating histone mark H3K4me3 in genes that are crucial for neutrophil activities.
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