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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon.

ABSTRACT: A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon.

PROVIDER: PRJNA890546 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21903103_1.fastq.gz	Fastqsanger.gz
	SRR21903103_2.fastq.gz	Fastqsanger.gz
	SRR21903104_1.fastq.gz	Fastqsanger.gz
	SRR21903104_2.fastq.gz	Fastqsanger.gz
	SRR21903105_1.fastq.gz	Fastqsanger.gz

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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon [iMO_Bcells_ECTV]

Project description:A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon [iMO_Bcells_ECTV]

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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon [iMO IFN ECTV]

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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon [iMO_Bcells_ECTV]

Project description:Inflammatory monocytes (iMO) and B-cells are the main targets of the poxvirus ectromelia virus (ECTV) in the lymph nodes of mice and play distinct roles in surviving the infection. Infected and bystander iMO control ECTV’s systemic spread, preventing early death, while B-cells make antibodies that eliminate ECTV. Our work demonstrates that within an infected animal that survives ECTV infection, intrinsic and bystander infection of iMO and B-cells differentially control the transcription of genes important for immune cell function and, perhaps, cell identity. Bystander cells upregulate metabolism, antigen presentation, and interferon-stimulated genes. Infected cells downregulate many cell-type-specific genes and upregulate transcripts typical of non-immune cells. Bys and Inf iMO non-redundantly contribute to the cytokine milieu and the interferon response. Furthermore, we uncovered how IFN-I or IFN-γ signaling differentially regulates immune pathways in Inf and Bys iMO and, that at steady state, IFN-I primes iMO for rapid IFN-I production and antigen presentation.

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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon [iMO IFN ECTV]

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A divergent and complementary transcriptional response in poxvirus-infected and bystander inflammatory monocytes is partly dictated by interferon.

Project description:This SuperSeries is composed of the SubSeries listed below.

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Interferon partly dictates a divergent transcriptional response in poxvirus-infected and bystander inflammatory monocytes.

Project description:Inflammatory monocytes (iMOs) and B cells are the main targets of the poxvirus ectromelia virus (ECTV) in the lymph nodes of mice and play distinct roles in surviving the infection. Infected and bystander iMOs control ECTV's systemic spread, preventing early death, while B cells make antibodies that eliminate ECTV. Our work demonstrates that within an infected animal that survives ECTV infection, intrinsic and bystander infection of iMOs and B cells differentially control the transcription of genes important for immune cell function and, perhaps, cell identity. Bystander cells upregulate metabolism, antigen presentation, and interferon-stimulated genes. Infected cells downregulate many cell-type-specific genes and upregulate transcripts typical of non-immune cells. Bystander (Bys) and infected (Inf) iMOs non-redundantly contribute to the cytokine milieu and the interferon response. Furthermore, we uncover how type I interferon (IFN-I) or IFN-γ signaling differentially regulates immune pathways in Inf and Bys iMOs and that, at steady state, IFN-I primes iMOs for rapid IFN-I production and antigen presentation.

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