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Recruitment of dendritic cell progenitors to foci of influenza A virus infection sustains immunity

ABSTRACT: Recruitment of dendritic cell progenitors to foci of influenza A virus infection sustains immunity

PROVIDER: PRJNA762088 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15833419.fastq.gz	Fastqsanger.gz
	SRR15833420.fastq.gz	Fastqsanger.gz
	SRR15833421.fastq.gz	Fastqsanger.gz
	SRR15833422.fastq.gz	Fastqsanger.gz

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Recruitment of dendritic cell progenitors to foci of influenza A virus infection sustains immunity.

Project description:Protection from infection with respiratory viruses such as influenza A virus (IAV) requires T cell–mediated immune responses initiated by conventional dendritic cells (cDCs) that reside in the respiratory tract. Here, we show that effective induction of T cell responses against IAV in mice requires reinforcement of the resident lung cDC network by cDC progenitors. We found that CCR2-binding chemokines produced during IAV infection recruit pre-cDCs from blood and direct them to foci of infection, increasing the number of progeny cDCs next to sites of viral replication. Ablation of CCR2 in the cDC lineage prevented this increase and resulted in a deficit in IAV-specific T cell responses and diminished resistance to reinfection. These data suggest that the homeostatic network of cDCs in tissues is insufficient for immunity and reveal a chemokine-driven mechanism of expansion of lung cDC numbers that amplifies T cell responses against respiratory viruses.

| S-EPMC7612017 | biostudies-literature

Recruitment of dendritic cell progenitors to foci of influenza A virus infection sustains immunity

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Gene expression signatures for Normal-looking, fibrotic foci and hyperplastic (adjacent to fibrotic foci) area in IPF lungs

Project description:To further understand the pathologic microenvironment in IPF, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish normal and IPF lung in normal-looking, fibrotic foci and hyperplastic areas of IPF lung. Four IPF lungs were dissected into normal-looking, fibrotic foci and hyperplastic areas by Laser-Capture-Microdissection. Gene expression analysis showed that 638 significantly different genes were identified that clearly distinguished the different IPF microenvironments . Among them, MMP19 was revealed as one of the most significantly up-regulated genes that distinguished normal looking epithelial cells (N) to hyperplastic epithelial cells, MMP19 up-regulation in IPF lungs was verified by immunohistochemical (IHC), qRT-PCR and Western-blot. IPF lungs are heterogeneity complex, which comprise normal looking area, fibrotic foci and hyperplastic area. In this study we separated the normal, fibrotic foci and hyperplastic area by LCM and employed Agilent whole genome gene expression microarray profiling to identify genes with the potential to distinguish the unique microenironment of IPF

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Fusarium oxysporum strain:FoCI-2

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Project description:To compare the gene expression profiles of Macrophage & Dendritic cell Progenitors (MDPs), Common Dendritic cell Progenitors (CDPs), committed dendritic cell precursors (pre-DCs), and Ly6Chi monocytes from mouse bone marrow Four samples (MDPs, CDPs, pre-DCs, and monocytes) were collected in triplicate

2012-04-25 | E-GEOD-37566 | biostudies-arrayexpress

The DEAD box helicase RDE-12 promotes amplification of RNAi in cytoplasmic foci in C. elegans

Project description:RNA interference (RNAi) is a potent mechanism for down-regulating gene expression. Conserved RNAi pathway components are found in animals, plants, fungi and other eukaryotes. In C. elegans, the RNAi response is greatly amplified by the synthesis of abundant secondary siRNAs. Exogenous double stranded RNA is processed by Dicer and RDE-1/Argonaute into primary siRNA that guides target mRNA recognition. The RDE-10/RDE-11 complex and the RNA dependent RNA polymerase RRF-1 then engage the target mRNA for secondary siRNA synthesis. However, the molecular link between primary siRNA production and secondary siRNA synthesis remains largely unknown. Furthermore, it is unclear if the sub-cellular sites for target mRNA recognition and degradation coincide with sites where siRNA synthesis and amplification occur. In the C. elegans germline, cytoplasmic P granules at the nuclear pores and perinuclear Mutator foci contribute to target mRNA surveillance and siRNA amplification, respectively. We report that RDE-12, a conserved FG domain containing DEAD-box helicase, localizes in P-granules and cytoplasmic foci that are enriched in RSD-6 but are excluded from the Mutator foci. Our results suggest that RDE-12 promotes secondary siRNA synthesis by orchestrating the recruitment of RDE-10 and RRF-1 to primary siRNA targeted mRNA in distinct cytoplasmic compartments. Examination of exogenous dsRNA trigger derived siRNA in wildtype and rde-12 mutant animals

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Dendritic cell and monocyte progenitors

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