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Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (bulk TCR-Seq)

ABSTRACT: Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (bulk TCR-Seq)

PROVIDER: PRJNA1106826 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28863800_1.fastq.gz	Fastqsanger.gz
	SRR28863800_2.fastq.gz	Fastqsanger.gz
	SRR28863801_1.fastq.gz	Fastqsanger.gz
	SRR28863801_2.fastq.gz	Fastqsanger.gz
	SRR28863802_1.fastq.gz	Fastqsanger.gz

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Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (bulk TCR-Seq)

Project description:Immunotherapy advances have been hindered by difficulties tracking the behaviours of lymphocytes following antigen-signalling. Here we present the antigen-receptor signalling reporter (AgRSR) mouse to fate-map lymphocytes responding to antigen at specific times and locations, to determine the behaviour of T cells involved in the tumour immune response. Contrary to reports of ready egress of T cells out of the tumour, we find that intratumoral antigen-signalling traps CD8+ T cells in the tumour. These clonal populations expand and become increasingly exhausted over time. In contrast, antigen- signalled regulatory T cell (Treg) clonal populations readily recirculate out of the tumour. Consequently, intratumoral antigen-signalling acts as a gatekeeper to compartmentalize CD8+ T cell responses – even within the same clonotype, enabling immunity to confine exhaustion to a specific tissue site.

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Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (scRNA-Seq)

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Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (scRNA-Seq)

Project description:Intratumoral antigen-signalling traps CD8+ T cells to confine exhaustion to the tumour site (scRNA-Seq)

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NLRP3 deficiency reverts intratumoral T cell exhaustion

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Intratumoral antigen signaling traps CD8<sup>+</sup> T cells to confine exhaustion to the tumor site.

Project description:Immunotherapy advances have been hindered by difficulties in tracking the behaviors of lymphocytes after antigen signaling. Here, we assessed the behavior of T cells active within tumors through the development of the antigen receptor signaling reporter (AgRSR) mouse, fate-mapping lymphocytes responding to antigens at specific times and locations. Contrary to reports describing the ready egress of T cells out of the tumor, we find that intratumoral antigen signaling traps CD8+ T cells in the tumor. These clonal populations expand and become increasingly exhausted over time. By contrast, antigen-signaled regulatory T cell (Treg) clonal populations readily recirculate out of the tumor. Consequently, intratumoral antigen signaling acts as a gatekeeper to compartmentalize CD8+ T cell responses, even within the same clonotype, thus enabling exhausted T cells to remain confined to a specific tumor tissue site.

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