Journal
NATURE COMMUNICATIONS
Volume 10, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-10601-6
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Funding
- Francis Crick Institute - Cancer Research UK [FC001126]
- UK Medical Research Council [FC001126, MRC U117565642]
- Wellcome Trust [FC001126, 207503/Z/17/Z]
- European Research Council [294682-TB-PATH]
- Illumina Inc., San Diego, CA, USA
- MRC Centenary Award
- Royal Veterinary College
- MRC
- Asthma UK PhD studentship (2014-2017)
- London School of Hygiene & Tropical Medicine
- NHLI, Imperial College, London
- Intramural Research Program of the National Institutes of Allergy and Infectious Disease
- Baylor Institute of Immunology Research, Dallas, USA
- Francis Crick Institute [FC001101, FC001206, FC001220, FC001076, FC001129]
- Wellcome Trust [207503/Z/17/Z] Funding Source: Wellcome Trust
- MRC [MC_U117565642, MC_UP_1202/12, MC_U117597139] Funding Source: UKRI
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [ZIAAI001207, ZIAAI000579] Funding Source: NIH RePORTER
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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-gamma and IFN-inducible, IL-17-induced neutrophil- or allergy-associated gene expression. Type I IFN and IFN-gamma-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-gamma 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.
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