Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Local niche-derived immunosuppressive CXCR2+ cells impair antiviral immunity

ABSTRACT: The severity of symptoms after viral infection varies between individuals, yet the underlying mechanism remains poorly understood. We categorized mice with varying severity into recovering and non-recovering groups after infection of vesicular stomatitis virus (VSV). We revealed that non-recovering mice expressed higher levels of anti-inflammatory cytokines in the olfactory bulb (OB) where VSV initially expand. Importantly, CXCR2+ cells resembling immunosuppressive myeloid-derived suppressor cells (MDSCs) were more abundant in the OB of non-recovering mice than in that of recovering mice after VSV infection. Depleting CXCR2+ MDSC-like cells from the brain increased inflammatory responses and the animal’s survival after infection. Furthermore, site-specific labeling of cells derived from the skull-bone marrow (skull-BM) indicated that a significant fraction of CXCR2+ MDSC-like cells in the OB originate from the skull-BM. This study unveiled the lethal effects of CXCR2+ MDSC-like cells on local immune responses to viral infection, highlighting their therapeutic potential for antiviral defense.

ORGANISM(S): Mus musculus

PROVIDER: GSE292764 | GEO | 2026/09/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Local niche-derived immunosuppressive CXCR2+ cells impair antiviral immunity [RNA-seq]

Project description:The severity of symptoms after viral infection varies between individuals, yet the underlying mechanism remains poorly understood. We categorized mice with varying severity into recovering and non-recovering groups after infection of vesicular stomatitis virus (VSV). We revealed that non-recovering mice expressed higher levels of anti-inflammatory cytokines in the olfactory bulb (OB) where VSV initially expand. Importantly, CXCR2+ cells resembling immunosuppressive myeloid-derived suppressor cells (MDSCs) were more abundant in the OB of non-recovering mice than in that of recovering mice after VSV infection. Depleting CXCR2+ MDSC-like cells from the brain increased inflammatory responses and the animal’s survival after infection. Furthermore, site-specific labeling of cells derived from the skull-bone marrow (skull-BM) indicated that a significant fraction of CXCR2+ MDSC-like cells in the OB originate from the skull-BM. This study unveiled the lethal effects of CXCR2+ MDSC-like cells on local immune responses to viral infection, highlighting their therapeutic potential for antiviral defense.

2026-09-05 | GSE304197 | GEO

Modified method for differentiation of myeloid-derived suppressor cells in vitro enhances immunosuppressive ability via glutathione metabolism

Project description:Myeloid-derived suppressor cells (MDSCs), which accumulate in tumor bearers, are known to suppress anti-tumor immunity and thus promote tumor progression. MDSCs are considered a major cause of resistance against immune checkpoint inhibitors in patients with cancer. Therefore, MDSCs are potential targets in cancer immunotherapy. In this study, we modified an in vitro method of MDSC differentiation. Upon stimulating bone marrow (BM) cells with granulocyte-macrophage colony-stimulating factor in vitro, we obtained both lymphocyte antigen 6G positive (Ly-6G+) and negative (Ly-6G−) MDSCs (collectively, hereafter referred to as conventional MDSCs), which were non-immunosuppressive and immunosuppressive, respectively. We then found that MDSCs differentiated from Ly-6G− BM (hereafter called 6G− BM-MDSC) suppressed T-cell proliferation more strongly than conventional MDSCs, whereas the cells differentiated from Ly-6G+ BM (hereafter called 6G+ BM-MDSC) were non-immunosuppressive. In line with this, conventional MDSCs or 6G− BM-MDSC, but not 6G+ BM-MDSC, promoted tumor progression in tumor-bearing mice. Moreover, we identified that activated glutathione metabolism was responsible for the enhanced immunosuppressive ability of 6G− BM-MDSC. Finally, we showed that Ly-6G+ cells in 6G− BM-MDSC, which exhibited weak immunosuppression, expressed higher levels of Cybb mRNA, an immunosuppressive gene of MDSCs, than 6G+ BM-MDSC. Together, these data suggest that the depletion of Ly-6G+ cells from the BM cells leads to differentiation of immunosuppressive Ly-6G+ MDSCs. In summary, we propose a better method for MDSC differentiation in vitro. Moreover, our findings contribute to the understanding of MDSC subpopulations and provide a basis for further research on MDSCs.

2023-01-10 | GSE218704 | GEO

Lymphoid structures in the skull bone marrow control homeostatic and anti-tumor immune responses in the CNS [dura/skull/sternum]

Project description:Accumulating evidence demonstrates that the central nervous system (CNS) is not disconnected from the peripheral immune system; however, precisely how the adaptive immune system surveils the CNS remains a critical question. Recent findings reveal that channels between the dura mater and the skull facilitate the exchange of cerebrospinal fluid and immune cells between the CNS and skull bone marrow (BM) under both homeostatic and disease conditions. Skull BM serves as a source of innate immune cells for the CNS, yet its role in adaptive immune responses remains insufficiently characterized. Here, we identify lymphoid structures within the skull BM, featuring germinal center-like formations and harboring a distinct population of follicular helper-like T cells that promote B cell activation and humoral immunity through CD40L, IL-21, and IFN-γ signaling. Adaptive immune cells within these skull BM lymphoid structures surveil and respond to CNS-derived antigens, which we demonstrate to be critical for optimal antitumor immunity in murine brain cancer models. Our discovery of distinct anatomical sites in the skull BM that enable adaptive immunosurveillance of the CNS highlights promising avenues for immunotherapies targeting neurological diseases, including brain cancers.

2026-07-13 | GSE313969 | GEO

Lymphoid structures in the skull bone marrow control homeostatic and anti-tumor immune responses in the CNS [skull/sternum]

2026-07-13 | GSE309634 | GEO

Lymphoid structures in the skull bone marrow control homeostatic and anti-tumor immune responses in the CNS [skull/brain]

2026-07-13 | GSE309632 | GEO

Mouse-adapted SARS-CoV-2 infected lungs from lean or obese ob/ob mice

Project description:Lean or obese C57BL/6JHamSlc-ob/ob (ob/ob) were developed continuous leptin (or vehicle) treatment for 6 weeks. Lung samples were generated from male mice of lean or obese ob/ob on 3 days post infection of mouse-adapted SARS-CoV-2.

2023-05-15 | E-MTAB-12623 | biostudies-arrayexpress

Mouse-adapted SARS-CoV-2 infected Lungs from wild type or genetically obese mice

Project description:Lung samples were generated from male mice of C57BL/6J(B6), C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2

2023-05-15 | E-MTAB-12617 | biostudies-arrayexpress

Lung samples from obese mice with or without mouse-adapted SARS-CoV-2 infection

Project description:Lung samples were generated from male mice of C57BL/6JHamSlc-ob/ob (ob/ob) and C57BLKS/J-db/db on 3 days post infection of mouse-adapted SARS-CoV-2 or non-infected condition

2023-05-15 | E-MTAB-12618 | biostudies-arrayexpress

TNFα-induced alterations in stromal progenitors in CML BM result in enhanced LSC growth via CXCL1-CXCR2 signaling

Project description:Leukemia stem cells (LSC) are not eradicated in chronic myeloid leukemia (CML) patients responding to tyrosine kinase inhibitor treatment. Bone marrow (BM) mesenchymal niches play an essential role in hematopoietic stem cell (HSC) maintenance. Here, we examined leukemia-induced alterations in mesenchymal progenitor populations using a murine CML model. 6C3+ stroma-forming progenitors were increased in CML BM, and demonstrated enhanced LSC but reduced HSC support compared to their normal counterparts. CML 6C3 cells showed enhanced TNFa-related gene signatures, and upregulated CXCL1 expression. TNFα signaling contributed to expansion and increased CXCL1 expression by 6C3 cells in CML BM. The CXCL1 receptor CXCR2 was upregulated in in LSC, and CXCR2 inhibition significantly reduced LSC growth both in vitro and in vivo. In conclusion, TNFα-induced alterations in stromal progenitors in CML BM result in enhanced CML LSC growth via CXCL1-CXCR2 signaling. Targeting this axis represents a novel therapeutic strategy to inhibit BM niche-protected LSC.

2021-06-16 | GSE126547 | GEO

Expression data from uninfected and VSV-infected Drosophila cells at 4 hours post-infection

Project description:Expression profiling of rapidly-induced genes upon VSV infection at 4 hours post-infection in Drosophila cells Drosophila cells were treated with Bgal dsRNA and either treated as uninfected or infected with VSV (MOI 10) for 4 hours, in two independent biological replicates. Total RNA was isolated using Trizol and microarray experiments were performed at the University of Pennsylvania Microarray Facility (U. Penn MF) following directions according to the manufacturerM-bM-^@M-^Ys protocol (Affymetrix). In brief, 100 ng RNA were amplified with the Ovation RNA Amplification System v2 (NuGen), the Encore Biotin Module (NuGen) was used for fragmentation and labeling, Protocol FS450 002 was used for hybridization, washing, and staining. Images were scanned using the GeneChipM-BM-. Scanner 3000 and image analysis was performed using the AffymetrixM-BM-. GeneChipM-BM-. Command ConsoleM-BM-. Software (AGCC).

2012-10-18 | E-GEOD-41146 | biostudies-arrayexpress

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