原创力文档type i interferons promote fatal immunopathology by regulating inflammatory monocytes and neutrophils during candida infectionsi型干扰素促进致命的免疫病理反应通过调节炎症单核细胞和中性粒细胞在念珠菌感染.pdfVIP
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type i interferons promote fatal immunopathology by regulating inflammatory monocytes and neutrophils during candida infectionsi型干扰素促进致命的免疫病理反应通过调节炎症单核细胞和中性粒细胞在念珠菌感染
Type I Interferons Promote Fatal Immunopathology by
Regulating Inflammatory Monocytes and Neutrophils
during Candida Infections
1 1 1 2 3
Olivia Majer , Christelle Bourgeois , Florian Zwolanek , Caroline Lassnig , Dontscho Kerjaschki ,
4 ¨ 2 1
Matthias Mack , Mathias Muller , Karl Kuchler *
1 Medical University Vienna - Max F. Perutz Laboratories, Christian Doppler Laboratory for Infection Biology, Campus Vienna Biocenter, Vienna, Austria, 2 University of
Veterinary Medicine Vienna, Institute of Animal Breeding and Genetics Biomodels Austria, Vienna, Austria, 3 Medical University of Vienna – Clinical Institute of Pathology,
AKH - General Hospital of Vienna, Vienna, Austria, 4 University Hospital of Regensburg, Internal Medicine II – Nephrology, Regensburg, Germany
Abstract
Invasive fungal infections by Candida albicans (Ca) are a frequent cause of lethal sepsis in intensive care unit patients. While
a contribution of type I interferons (IFNs-I) in fungal sepsis remains unknown, these immunostimulatory cytokines mediate
the lethal effects of endotoxemia and bacterial sepsis. Using a mouse model lacking a functional IFN-I receptor (Ifnar12/ 2),
we demonstrate a remarkable protection against invasive Ca infections. We discover a mechanism whereby IFN-I signaling
controls the recruitment of inflammatory myeloid cells, including Ly6Chi monocytes and neutrophils, to infected kidneys by
driving expression of the chemokines CCL2 and KC. Within kidneys, monocytes differentiate into inflammatory DCs but fail
to functionally mature in Ifnar12/ 2 mice, as demonstrated by the impaired upregulation of the key activation markers
PDCA1 and iNOS. The increased acti
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