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Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

ABSTRACT: Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

PROVIDER: PRJNA1136005 | ENA |

REPOSITORIES: ENA

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Effect of recombinant IGLL5 treatment on gene expressing of high endothelial venules

Project description:High endothelial venules (HEVs) are key component in the formation of tertiary lymphatic structure. Our previous studies have shown that IGLL5+B cells adhere to and inhibit the functional phenotype of HEVs. In addition, we found that IGLL5 binds to the LTβR receptor on the membrane of HEVs.

2025-08-01 | GSE272276 | GEO

Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

Project description:High endothelial venules (HEVs) are specialized post-capillary venules that recruit naïve lymphocytes to the lymph nodes and are essential for the development of adaptive immunity. HEVs can also develop in tumors. These specialized tumor vessels are thought to be important for recruiting naïve T cells and B cells into tumors and locally enhancing anti-tumor immunity by supporting the formation of tertiary lymphoid structures. By a comparative transcriptome analysis in human breast cancer, we investigated differentially expressed genes between tumor-associated HEVs and the rest of the tumor vasculature. Tumor vessels highly expressing HEV-upregulated genes, such as the homeobox gene MEOX2 and the tetraspanin gene TSPAN7, were associated with extensive infiltration of T and B lymphocytes and the occurrence of tertiary lymphoid structures, which is known to predict therapeutic responses to immune checkpoint inhibitors. Moreover, high transcript counts of these genes in clinical tumor specimens were associated with a significant survival benefit in advanced breast cancer. The molecular signature of HEVs identified here may be useful for guiding immunotherapies and provide a new direction for investigating tumor-associated HEVs and their clinical significance.

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Transcriptome Analysis of Tumor Associated High Endothelial Venules in Breast Cancer

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

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

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

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.

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

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Single-cell analysis reveals heterogeneity of high endothelial venules and different regulation of genes controlling lymphocyte entry to lymph nodes

Project description:High endothelial venules (HEVs) are specialized blood vessels allowing recirculation of naïve lymphocytes through lymphoid organs. Here, using full length single-cell RNA sequencing, RNA-FISH, flow cytometry and immunohistofluorescence, we reveal the heterogeneity of HEVs in adult mouse peripheral lymph nodes (PLNs) under conditions of homeostasis, antigenic stimulation and after inhibition of lymphotoxin-b receptor (LTbR) signaling. We demonstrate that HEV endothelial cells are in an activated state during homeostasis, and we identify the genes characteristic of the differentiated HEV phenotype. We show that LTbR signaling regulates many HEV genes and pathways in resting PLNs, and that immune stimulation induces a global and temporary inflammatory phenotype in HEVs without compromising their ability to recruit naïve lymphocytes. Most importantly, we uncover differences in the regulation of genes controlling lymphocyte trafficking, Glycam1, Fut7, Gcnt1, Chst4, B3gnt3 and Ccl21a, that have implications for HEV function and regulation in health and disease.

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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

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