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Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

ABSTRACT: Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

PROVIDER: PRJNA407766 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6048630_1.fastq.gz	Fastqsanger.gz
	SRR6048630_2.fastq.gz	Fastqsanger.gz
	SRR6048631_1.fastq.gz	Fastqsanger.gz
	SRR6048631_2.fastq.gz	Fastqsanger.gz
	SRR6048632_1.fastq.gz	Fastqsanger.gz

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Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

Project description:T follicular helper (Tfh) cells are a subset of CD4+ T cells that promote antibody production during vaccination. Conventional dendritic cells (cDCs) efficiently prime Tfh cells; however, conclusions regarding the nature of the cDC responsible for instructing Tfh cell differentiation have differed between recent studies. We found that these discrepancies might exist, in part, due to the unusual sites used for immunization in murine models, which differentially bias which DC subsets access antigen. We used intranasal immunization as a physiologically relevant route of exposure that we show delivers antigen to all tissue DC subsets. Using a combination of mice in which the function of individual DC subsets is impaired and different formulations of antigen delivery, we determined that CD11b+ migratory type 2 conventional DCs (cDC2s) are necessary and sufficient for Tfh induction. DC-specific deletion of the guanine nucleotide exchange factor DOCK8 resulted in an isolated loss of CD11b+ cDC2 but not CD103+ cDC1 migration to lung-draining lymph nodes. Impaired cDC2 migration or development in DC-specific Dock8 or Irf4 knockout mice, respectively, led to reduced Tfh cell and antibody development, whereas loss of CD103+ cDC1s in Batf3-/- mice did not. Loss of cDC2-mediated Tfh responses was associated with impaired antibody-mediated protection from live influenza virus challenge. We show that migratory cDC2s uniquely carry antigen into the sub-anatomic regions of the lymph node where Tfh cell priming occurs, the T-B border. This work identifies the DC responsible for Tfh cell-dependent antibody responses, in particular when antigen dose is limiting or is encountered at a mucosal site, which could ultimately inform the formulation and delivery of vaccines.

2017-12-01 | GSE103956 | GEO

Migratory CD11b+ conventional dendritic cells induce T follicular helper cell-dependent antibody responses.

Project description:T follicular helper (Tfh) cells are a subset of CD4+ T cells that promote antibody production during vaccination. Conventional dendritic cells (cDCs) efficiently prime Tfh cells; however, conclusions regarding which cDC instructs Tfh cell differentiation have differed between recent studies. We found that these discrepancies might exist because of the unusual sites used for immunization in murine models, which differentially bias which DC subsets access antigen. We used intranasal immunization as a physiologically relevant route of exposure that delivers antigen to all tissue DC subsets. Using a combination of mice in which the function of individual DC subsets is impaired and different antigen formulations, we determined that CD11b+ migratory type 2 cDCs (cDC2s) are necessary and sufficient for Tfh induction. DC-specific deletion of the guanine nucleotide exchange factor DOCK8 resulted in an isolated loss of CD11b+ cDC2, but not CD103+ cDC1, migration to lung-draining lymph nodes. Impaired cDC2 migration or development in DC-specific Dock8 or Irf4 knockout mice, respectively, led to reduced Tfh cell priming, whereas loss of CD103+ cDC1s in Batf3-/- mice did not. Loss of cDC2-dependent Tfh cell priming impaired antibody-mediated protection from live influenza virus challenge. We show that migratory cDC2s uniquely carry antigen into the subanatomic regions of the lymph node where Tfh cell priming occurs-the T-B border. This work identifies the DC subset responsible for Tfh cell-dependent antibody responses, particularly when antigen dose is limiting or is encountered at a mucosal site, which could ultimately inform the formulation and delivery of vaccines.

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Transcription profiling of WT and NFAT2 KO follicular helper CD4 T cells and non follicular helper CD4 T cell populations

Project description:Comparatative gene expression analysis for wild type and NFAT2-/- CD4 T cell subsets including follicular helper CD4+ T (TFH) cells, activated CD4+ T cells, and naive CD4+ T cells isolated from the spleen.

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Mll1 in T follicular helper cell differentiation

Project description:Mll1 in T follicular helper cell differentiation

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