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Journal article

Absence of GP130 cytokine receptor signaling causes extended Stüve-Wiedemann syndrome

Abstract:
The gene IL6ST encodes GP130, the common signal transducer of the IL-6 cytokine family consisting of 10 cytokines. Previous studies have identified cytokine-selective IL6ST defects that preserve LIF signaling. We describe three unrelated families with at least five affected individuals who presented with lethal Stüve-Wiedemann-like syndrome characterized by skeletal dysplasia and neonatal lung dysfunction with additional features such as congenital thrombocytopenia, eczematoid dermatitis, renal abnormalities, and defective acute-phase response. We identified essential loss-of-function variants in IL6ST (a homozygous nonsense variant and a homozygous intronic splice variant with exon skipping). Functional tests showed absent cellular responses to GP130-dependent cytokines including IL-6, IL-11, IL-27, oncostatin M (OSM), and leukemia inhibitory factor (LIF). Genetic reconstitution of GP130 by lentiviral transduction in patient-derived cells reversed the signaling defect. This study identifies a new genetic syndrome caused by the complete lack of signaling of a whole family of GP130-dependent cytokines in humans and highlights the importance of the LIF signaling pathway in pre- and perinatal development.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1084/jem.20191306

Authors


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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDM
Sub department:
NDM Experimental Medicine
Role:
Author


Publisher:
Rockefeller University Press
Journal:
Journal of Experimental Medicine More from this journal
Volume:
217
Issue:
3
Article number:
e20191306
Publication date:
2020-01-08
Acceptance date:
2019-11-14
DOI:
EISSN:
1540-9538
ISSN:
0022-1007


Language:
English
Pubs id:
pubs:1081478
UUID:
uuid:2ea9a15c-6b74-4594-9612-16d12bf7a274
Local pid:
pubs:1081478
Source identifiers:
1081478
Deposit date:
2020-01-10

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