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Identification of B-cell specific checkpoint molecules regulating anti-tumor immunity

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

ORGANISM(S): Mus musculus

PROVIDER: GSE225717 | GEO | 2023/06/22

REPOSITORIES: GEO

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Identification of B-cell specific checkpoint molecules regulating anti-tumor immunity

Project description:Identification of B-cell specific checkpoint molecules regulating anti-tumor immunity

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Single-cell RNA-seq for identification of B-cell specific checkpoint molecules regulating anti-tumor immunity

Project description:The role of B cells in anti-tumor immunity is still debated and accordingly, most therapies have focused on targeting T and NK cells to inhibit tumor growth1,2. Here, using high-throughput flow cytometry, bulk and single-cell RNA- and BCR-sequencing of B cells temporally during B16F10 melanoma growth, we identified a subset of B cells that expands specifically in the draining lymph node over time in tumor bearing-mice. The expanding B cell subset expresses the cell surface molecule T cell immunoglobulin and mucin domain 1 (TIM-1) and a unique transcriptional signature, including multiple co-inhibitory molecules such as PD-1, TIM-3, TIGIT and LAG-3. While conditional deletion of these co-inhibitory molecules on B cells had little or no effect on tumor burden, selective deletion of Havcr1 (the gene encoding TIM-1) in B cells both dramatically inhibited tumor growth and enhanced effector T cell responses. Loss of TIM-1 enhanced the type 1 interferon response in B cells, which augmented B cell activation and increased antigen presentation and co-stimulation, resulting in increased expansion of tumor-specific effector T cells. Our results demonstrate that manipulation of TIM-1-expressing B cells enables engagement of the second arm of adaptive immunity to promote anti-tumor immunity and inhibit tumor growth.

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Bulk RNA-seq for B-cell specific checkpoint molecules regulating anti-tumor immunity

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B-cell-specific checkpoint molecules that regulate anti-tumour immunity.

Project description:The role of B cells in anti-tumour immunity is still debated and, accordingly, immunotherapies have focused on targeting T and natural killer cells to inhibit tumour growth1,2. Here, using high-throughput flow cytometry as well as bulk and single-cell RNA-sequencing and B-cell-receptor-sequencing analysis of B cells temporally during B16F10 melanoma growth, we identified a subset of B cells that expands specifically in the draining lymph node over time in tumour-bearing mice. The expanding B cell subset expresses the cell surface molecule T cell immunoglobulin and mucin domain 1 (TIM-1, encoded by Havcr1) and a unique transcriptional signature, including multiple co-inhibitory molecules such as PD-1, TIM-3, TIGIT and LAG-3. Although conditional deletion of these co-inhibitory molecules on B cells had little or no effect on tumour burden, selective deletion of Havcr1 in B cells both substantially inhibited tumour growth and enhanced effector T cell responses. Loss of TIM-1 enhanced the type 1 interferon response in B cells, which augmented B cell activation and increased antigen presentation and co-stimulation, resulting in increased expansion of tumour-specific effector T cells. Our results demonstrate that manipulation of TIM-1-expressing B cells enables engagement of the second arm of adaptive immunity to promote anti-tumour immunity and inhibit tumour growth.

| S-EPMC10795478 | biostudies-literature

Bulk RNA-seq for B-cell specific checkpoint molecules regulating anti-tumor immunity

Project description:Bulk RNA-seq for B-cell specific checkpoint molecules regulating anti-tumor immunity

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Single-cell RNA-seq for identification of B-cell specific checkpoint molecules regulating anti-tumor immunity

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Project description:This SuperSeries is composed of the SubSeries listed below.

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LSD1 Ablation Stimulates Anti-tumor Immunity and Enables Checkpoint Blockade.

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