Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE217454 | GEO | 2026/03/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [III]

Project description:High-endothelial-venules (HEVs) offer another entry point for tumor metastasis in mice. To investigate whether HEVs and non-specialized blood vessels exert different effects on disseminating tumor cells, we enriched EO771 derivatives HEVM3 (preferentially metastasize through HEVs) cells and BVM3 (preferentially metastasize through blood vessels) cells. To explore how HEVs regulate immunogenicity of tumor cells, we compared the transcriptomes of BECs isolated from mammary blood vessels and HECs isolated from lymph nodes of mice inoculated with or without EO771-HEVM3 tumors. We demonstrated that ALOX12 specifically expressed in HEVs in LNs induces immune evasion of neighboring tumor cells by 12-HETE. To identify the factor(s) that upregulate ALOX12, we compared the mRNA transcriptomes between EO771-HEVM3 cells and EO771-BVM3 cells. To explore how 12-HETE promotes immune evasion of tumor cells, we performed total RNA-seq analysis in EO771 cells after 12-HETE treatment.

2026-03-01 | GSE245061 | GEO

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [II]

2026-03-01 | GSE217453 | GEO

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [I]

2026-03-01 | GSE216939 | GEO

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [Metastatic lymph node]

2026-03-01 | GSE306742 | GEO

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12

Project description:Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12

| PRJNA899035 | ENA

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [III]

Project description:Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [III]

| PRJNA1026880 | ENA

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [II]

Project description:Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [II]

| PRJNA899043 | ENA

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [I]

Project description:Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [I]

| PRJNA896209 | ENA

Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [Metastatic lymph node]

Project description:Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12 [Metastatic lymph node]

| PRJNA1312017 | ENA

Neutrophils recruited through high endothelial venules of the lymph nodes via PNAd intercept disseminating <i>Staphylococcus aureus</i>.

Project description:Staphylococcus aureus is a skin- and respiratory tract-colonizing bacterium and is the leading cause of community-acquired skin infections. Dissemination of these bacteria into systemic circulation causes bacteremia, which has a high mortality rate. Therefore, understanding the immunologic barriers that prevent dissemination is critical to developing novel treatments. In this study, we demonstrate that an S. aureus breach across skin leads to some migration of the pathogen to the draining lymph node, but no further. While subcapsular sinus (SCS) macrophage in lymph nodes were important in detaining S. aureus, a rapid complement-dependent neutrophil recruitment (independent of the SCS macrophage) via high endothelial venules (HEVs) resulted in high numbers of neutrophils that intercepted the bacteria in the lymph nodes. Peripheral Node Addressin together with its two ligands, L-selectin and platelet P-selectin, are critical for recruiting neutrophils via the HEVs. Almost no neutrophils entered the lymph nodes via lymphatics. Neutrophils actively phagocytosed S. aureus and helped sterilize the lymph nodes and prevent dissemination to blood and other organs.

| S-EPMC5877924 | biostudies-literature

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