Imperial College London
Alternate

ProfessorClareLloyd

Faculty of Medicine, National Heart & Lung Institute

Interim Head of NHLI, Vice-Dean (institutional Affairs) FoM
 
 
 
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Contact

 

+44 (0)20 7594 3102c.lloyd Website

 
 
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Location

 

Office 352Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Singhania:2019:10.1038/s41467-019-10601-6,
author = {Singhania, A and Graham, CM and Gabrysova, L and Moreira-Teixeira, L and Stavropoulos, E and Pitt, JM and Chakravarty, P and Warnatsch, A and Branchett, WJ and Conejero, L and Lin, J-W and Davidson, S and Wilson, MS and Bancroft, G and Langhorne, J and Frickel, E and Sesay, AK and Priestnall, SL and Herbert, E and Ioannou, M and Wang, Q and Humphreys, IR and Dodd, J and Openshaw, PJM and Mayer-Barber, KD and Jankovic, D and Sher, A and Lloyd, CM and Baldwin, N and Chaussabel, D and Papayannopoulos, V and Wack, A and Banchereau, JF and Pascual, VM and O'Garra, A},
doi = {10.1038/s41467-019-10601-6},
journal = {Nature Communications},
title = {Transcriptional profiling unveils type I and II interferon networks in blood and tissues across diseases},
url = {http://dx.doi.org/10.1038/s41467-019-10601-6},
volume = {10},
year = {2019}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Understanding how immune challenges elicit different responses is critical for diagnosing and deciphering immune regulation. Using a modular strategy to interpret the complex transcriptional host response in mouse models of infection and inflammation, we show a breadth of immune responses in the lung. Lung immune signatures are dominated by either IFN-γ and IFN-inducible, IL-17-induced neutrophil- or allergy-associated gene expression. Type I IFN and IFN-γ-inducible, but not IL-17- or allergy-associated signatures, are preserved in the blood. While IL-17-associated genes identified in lung are detected in blood, the allergy signature is only detectable in blood CD4+ effector cells. Type I IFN-inducible genes are abrogated in the absence of IFN-γ signaling and decrease in the absence of IFNAR signaling, both independently contributing to the regulation of granulocyte responses and pathology during Toxoplasma gondii infection. Our framework provides an ideal tool for comparative analyses of transcriptional signatures contributing to protection or pathogenesis in disease.
AU  - Singhania,A
AU  - Graham,CM
AU  - Gabrysova,L
AU  - Moreira-Teixeira,L
AU  - Stavropoulos,E
AU  - Pitt,JM
AU  - Chakravarty,P
AU  - Warnatsch,A
AU  - Branchett,WJ
AU  - Conejero,L
AU  - Lin,J-W
AU  - Davidson,S
AU  - Wilson,MS
AU  - Bancroft,G
AU  - Langhorne,J
AU  - Frickel,E
AU  - Sesay,AK
AU  - Priestnall,SL
AU  - Herbert,E
AU  - Ioannou,M
AU  - Wang,Q
AU  - Humphreys,IR
AU  - Dodd,J
AU  - Openshaw,PJM
AU  - Mayer-Barber,KD
AU  - Jankovic,D
AU  - Sher,A
AU  - Lloyd,CM
AU  - Baldwin,N
AU  - Chaussabel,D
AU  - Papayannopoulos,V
AU  - Wack,A
AU  - Banchereau,JF
AU  - Pascual,VM
AU  - O'Garra,A
DO  - 10.1038/s41467-019-10601-6
PY  - 2019///
SN  - 2041-1723
TI  - Transcriptional profiling unveils type I and II interferon networks in blood and tissues across diseases
T2  - Nature Communications
UR  - http://dx.doi.org/10.1038/s41467-019-10601-6
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000473132200051&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/71894
VL  - 10
ER  -
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