Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lung dendritic cells migrate to the spleen to prime long-lived memory CD8+ T cell precursors after influenza virus infection

ABSTRACT: Lung dendritic cells migrate to the spleen to prime long-lived memory CD8+ T cell precursors after influenza virus infection

PROVIDER: PRJNA746235 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15116437_1.fastq.gz	Fastqsanger.gz
	SRR15116437_2.fastq.gz	Fastqsanger.gz
	SRR15116438_1.fastq.gz	Fastqsanger.gz
	SRR15116438_2.fastq.gz	Fastqsanger.gz
	SRR15116439_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Lung dendritic cells migrate to the spleen to prime long-lived memory CD8+ T cell precursors after influenza virus infection

Project description:CD8+ T cell responses to pulmonary challenges are primed by lung-migratory dendritic cells (mDCs), which capture antigens in the lung and migrate to the lung-draining mediastinal lymph node (med-LNs) to activate T cells. Notably, the lung and the spleen are not connected by the lymphatic vasculature. Thus, the current paradigm suggests that the med-LN is the only site for T cell priming to viruses that are restricted to the respiratory tract. Our results challenge this “LN-centric” paradigm. Using an influenza virus infection, we show here that lung-mDCs egress the med-LN and traffic to the spleen, where they prime influenza-specific CD8+ T cells. Importantly, CD8+ T cells primed in the spleen are transcriptionally different and have enhanced ability to differentiate into long-lived memory cells compared to med-LN-primed counterparts. Thus, our data reveal a previously ignored lung-mDC trafficking pathway that connects the lung with the spleen and has profound immunological implications.

2021-07-16 | GSE179995 | GEO

Lung dendritic cells migrate to the spleen to prime long-lived TCF1<sup>hi</sup> memory CD8<sup>+</sup> T cell precursors after influenza infection.

Project description:CD8+ T cell responses to pulmonary challenges are primed by lung migratory dendritic cells (mDCs), which capture antigens in the lungs and migrate to the lung-draining mediastinal lymph node (med-LN) to activate T cells. The lungs and the spleen are not connected by the lymphatic vasculature. Thus, the current paradigm suggests that, in response to respiratory virus infections that are restricted to the respiratory tract, priming of T cell responses by lung mDCs takes place entirely in the med-LN. Our results challenge this “LN-centric” paradigm by demonstrating that, during influenza virus infection, lung mDCs egress the med-LN and traffic to the spleen, where they prime influenza-specific CD8+ T cells. CD8+ T cells primed in the spleen are transcriptionally distinct and have enhanced ability to differentiate into long-lived memory cells compared with med-LN–primed counterparts. Thus, our data identify a lung mDC trafficking pathway that connects the lungs with the spleen.

| S-EPMC8559272 | biostudies-literature

KLRG1+ Memory CD8 T cells Combine Properties of Short-lived Effectors and Long-lived Memory

Project description:CD8 effector T cells with a CD127hi KLRG1- phenotype are considered precursors to the long-lived memory pool, while KLRG1+ CD127low cells are viewed as short-lived effectors. Nevertheless, we and others have shown that a KLRG1+ CD127low population persists into the memory phase and that these T cells (termed long-lived effector cells or LLEC) display robust protective function during acute re-challenge with bacteria or viruses. Whether these T cells represent a true memory population or are instead a remnant effector cell population that failed to undergo initial contraction has remained unclear. Here, we show that LLEC from mice express a distinct phenotypic and transcriptional signature that shares characteristics of both early effectors and long-lived memory cells. Furthermore, we find that LLEC are exclusively derived from day 12 KLRG1+ effector cells. Our work challenges the concept that the KLRG1+ CD127low population is dominated by short-lived cells and shows that KLRG1 downregulation is not a prerequisite to become a long-lived protective memory T cell.

2020-08-26 | GSE152841 | GEO

PPARg marks splenic precursors of multiple nonlymphoid-tissue Treg compartments [scRNA-seq spleen]

Project description:PPARg marks splenic precursors of multiple nonlymphoid-tissue Treg compartments [scRNA-seq spleen]

| PRJNA712996 | ENA

An inflammatory loop established between spleen-derived myeloid cells and CD4+ T cells leads to accumulation of long-lived plasma cells that exacerbate lupus autoimmunity

Project description:Splenic long-lived plasma cells (PCs) are abnormally numerous and deleterious in systemic autoimmune diseases, yet how they accumulate remains poorly understood. We demonstrate here that a pathological role of spleen-derived CD11b+Gr-1+ myeloid cells (SPMCs) underpins the accumulation of splenic long-lived PCs in a lupus-prone model. SPMCs were a mixture of granulocytic and monocytic myeloid-derived suppressor cells (MDSCs) that were expanded and acquired proinflammatory phenotypes in situ during lupus progression. By promoting the development of IFN--secreting and follicular helper T cells, SPMCs licensed CD4+ T cells to be pathologic activators of SPMCs and PCs. SPMCs also directly promoted the survival of PCs by providing B-cell activating factor of the TNF family. The frequency of SPMCs correlated with that of splenic long-lived PCs. Depletion of CD11b+Gr-1+ cells reduced autoantibody production. Thus, our findings suggest that SPMCs expanded in situ establish a positive feedback loop with CD4+ T cells, leading to accumulation of long-lived PCs which exacerbate lupus autoimmunity.

2021-02-09 | GSE161850 | GEO

Project description:Immune system aging contributes significantly to declining health with age. It is unknown to what extent human and mice immune systems go through similar age-related changes and whether there are conserved biomarkers of aging. We characterized age-related changes in the immune system of long (C57BL/6J) and short-lived (NZO/HILtJ) strains and compared them with blood-driven human aging signatures. Peripheral blood lymphocytes (PBL), spleen cells and spleen-driven naive and memory CD8+ T cells were profiled using flow cytometry, RNA-seq and ATAC-seq from young (3 months) and old (18 months) mice. Pro-inflammatory myeloid genes were activated with age across strains and tissues, echoing human 'inflammaging' signatures. ATAC-seq footprinting analyses uncovered increased binding of pro-inflammatory transcription factors with age (e.g., AP1 complex, NFKB signaling pathway). Machine learning models identified inflammation, cytotoxic, and naive T cell derived genes to be strong signatures of immunosenescence. These data are publicly shared as a resource for immune aging (https://immune-aging.jax.org/mice).

2021-12-01 | GSE159795 | GEO

2021-12-01 | GSE159794 | GEO

BAFF and CD4+ T cells are major survival factors for long-lived splenic plasma cells in a B-cell–depletion context

Project description:Previous data have suggested that B-cell–depletion therapy may induce the settlement of autoreactive long-lived plasma cells (LLPCs) in the spleen of patients with autoimmune cytopenia. To investigate this process, we used the AID-CreERT2-EYFP mouse model to follow PCs engaged in an immune response. Multiplex-PCR at the single-cell level revealed that only a small fraction of splenic PCs had a long-lived signature, whereas PCs present after anti-CD20 antibody treatment appeared more mature, similar to bone-marrow PCs. It suggested that, in addition to a process of selection, a maturation induced upon B-cell depletion drove PCs toward a long-lived program. We showed that BAFF and CD4+ T cells play a major role in PC survival niche, because combining anti-CD20 with anti-BAFF or anti-CD4 antibody greatly reduce the number of splenic PCs. Similar results were obtained in the lupus-prone NZB/W model. These different contributions of soluble and cellular components of the PC niche in the spleen demonstrate that the LLPC expression profile is not cell-intrinsic but largely depends on signals provided by the splenic microenvironment, implying that interfering with these components at the time of B cell depletion might improve the response rate in autoimmune cytopenia.

2018-02-19 | E-MTAB-6449 | biostudies-arrayexpress

Project description:Age-related changes in blood and spleen-derived immune cells in long and short lived mice strains

| PRJNA670496 | ENA

Temporal dynamics and genomic programming of plasma cell fates

Project description:Bone marrow plasma cells (BMPCs) of varying lifespans are generated through a germinal center response (GC). The developmental dynamics and genomic programs of antigen-specific plasma cell (PC) precursors remain to be elucidated. Using a model antigen, we demonstrate biphasic generation of BMPC precursors, with those generating long-lived PCs preferentially produced in late phase of GC response. Clonal tracing using scRNA-seq+BCR-seq in spleen and bone marrow compartments, coupled with adoptive transfer experiments, reveal a novel PC transition state that gives rise to functionally competent PC precursors, the latter undergo clonal expansion, dependent on inducible expression of TIGIT. We propose a model for the proliferation and programming of precursors of long-lived BMPCs, based on extended antigen encounters.

2024-02-01 | GSE240813 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data