About: During Aspergillus infection, neutrophil, monocyte-derived DC, and plasmacytoid DC enhance innate immune defense through CXCR3-dependent crosstalk

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About: During Aspergillus infection, neutrophil, monocyte-derived DC, and plasmacytoid DC enhance innate immune defense through CXCR3-dependent crosstalk Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	During Aspergillus infection, neutrophil, monocyte-derived DC, and plasmacytoid DC enhance innate immune defense through CXCR3-dependent crosstalk
Creator	Luster, Andrew Hohl, Tobias Rivera, Espinosa, Vanessa Gjonbalaj, Mergim Guo, Yahui Jhingran, Anupam Kasahara, Shinji Mills, Kathleen Tosini, Nicholas Zhai, Bing Aufiero, A
Source	BioRxiv
abstract	Aspergillus fumigatus, a ubiquitous mold, is a common cause of invasive aspergillosis (IA) in immunocompromised patients. Host defense against IA relies on lung-infiltrating neutrophils and monocyte-derived dendritic cells (Mo-DCs). Here, we demonstrate that plasmacytoid dendritic cells (pDCs), which are prototypically anti-viral cells, participate in innate immune crosstalk underlying mucosal antifungal immunity. Aspergillus-infected murine Mo-DCs and neutrophils recruited pDCs to the lung by releasing the CXCR3 ligands, CXCL9 and CXCL10, in a Dectin-1/Card9- and type I and III interferon-signaling dependent manner, respectively. During aspergillosis, circulating pDCs entered the lung in response to CXCR3-dependent signals. Via targeted pDC ablation, we found that pDCs were essential for host defense in the presence of normal neutrophil and Mo-DC numbers. Although interactions between pDC and fungal cells were not detected, pDCs regulated neutrophil NADPH oxidase activity and conidial killing. Thus, pDCs act as positive feedback amplifiers of neutrophil effector activity against inhaled mold conidia.
has issue date	2020-05-05(xsd:dateTime)
bibo:doi	10.1101/2020.05.05.079517
has license	biorxiv
sha1sum (hex)	ea7cf8a6044656111514065587a717016e0339e7
schema:url	https://doi.org/10.1101/2020.05.05.079517
resource representing a document's title	During Aspergillus infection, neutrophil, monocyte-derived DC, and plasmacytoid DC enhance innate immune defense through CXCR3-dependent crosstalk
schema:publication	bioRxiv
resource representing a document's body	covid:ea7cf8a6044656111514065587a717016e0339e7#body_text
is schema:about of	named entity 'Host' named entity 'CXCL9' named entity 'FOUND' named entity 'PDCS' named entity 'A COMMON' named entity 'CXCL10' named entity 'mucosal' named entity 'pDCs' named entity 'pDCs' named entity 'pDC' named entity 'cells' named entity 'innate immune' named entity 'signals' named entity 'presence' named entity 'patients' named entity 'numbers' named entity 'lung' named entity 'neutrophils' named entity 'Host defense' named entity 'murine' named entity 'Dectin' named entity 'innate immune' named entity 'immunocompromised patients' named entity 'antifungal' named entity 'crosstalk' named entity 'monocyte' named entity 'neutrophil' named entity 'Dectin-1' named entity 'hematoxylin and eosin' named entity 'lungs' named entity 'LDH' named entity 'ROS' named entity 'paraformaldehyde' named entity 'CD45' named entity 'dsRed' named entity 'neutrophil' named entity 'fungus' named entity 'pDCs' named entity 'pneumonia' named entity 'gene' named entity 'mice' named entity 'BDCA2' named entity 'CARD9' named entity 'pDC' named entity 'cytotoxicity' named entity 'Phagocyte' named entity 'germination' named entity 'CD11b' named entity 'albumin' named entity 'albumin' named entity 'Cxcr3' named entity 'fluorescence' named entity 'conidia' named entity 'Aspergillus' named entity 'lungs' named entity 'TaqMan' named entity 'pDCs' named entity 'conidial' named entity 'neutrophil' named entity 'neutrophil' named entity 'neutrophils' named entity 'Applied Biosystems' named entity 'receptor' named entity 'downregulated' named entity 'pDCs' named entity 'neutrophils' named entity 'mice' named entity 'effector' named entity 'CCR2' named entity 'neutrophils' named entity 'pDC' named entity 'infection' named entity 'reverse-transcribed'

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