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Evolutionary fingerprint in rodent PD1 confers weakened activity and enhanced tumor immunity compared to human PD1

ABSTRACT: Evolutionary fingerprint in rodent PD1 confers weakened activity and enhanced tumor immunity compared to human PD1

PROVIDER: PRJNA1180928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31190504_1.fastq.gz	Fastqsanger.gz
	SRR31190504_2.fastq.gz	Fastqsanger.gz
	SRR31190505_1.fastq.gz	Fastqsanger.gz
	SRR31190505_2.fastq.gz	Fastqsanger.gz
	SRR31190506_1.fastq.gz	Fastqsanger.gz

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Evolutionary fingerprint in rodent PD1 confers weakened activity and enhanced tumor immunity compared to human PD1

Project description:Mechanistic understanding of the immune checkpoint receptor PD1 is largely based on mouse models, but human and mouse PD1 orthologs exhibit only 59.6% identity in amino acid sequences, raising the question of potential cross-species functional differences. Based on our biochemical evidence that human PD1 is more inhibitory than mouse PD1, we addressed the functional consequence of PD1 humanization in a mouse melanoma model with adoptively transferred T cells. Using CITE-seq (cellular indexing of transcriptomes and epitopes by sequencing), we found that humanization of PD1 intracellular domain (ICD) in CD8 T cells decreases the numbers, effector functions, and differentiation of intratumoral T cells. Specifically, PD1 humanization reduced the number of effector-like exhausted T cell subset while increasing the precursor-exhausted T cell subset, the latter of which is known to respond to anti-PD(L)1 therapy.

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Project description:Functional impairment of the immune response to chronic viral infections and malignancies is characterised by exhausted T cells, which do not respond to antigen. The cell surface receptor PD1 has been implicated in the maintenance of T cell exhaustion and is an attractive target for immunomodulatory approaches to the treatment of such conditions. However, the mechanisms by which PD1 signalling causes exhaustion and the exact response of T cells to PD1 activation are not clear although it has been suggested that PD1 up regulates a number of anti-proliferative factors. Here we perform cytokine and transcriptional profiling of uninfected primary human T cells to characterise these events. We find that PD1 completely prevents cytokine and transcrip- tional changes induced by CD3/28 stimulation. We do not see any factors specifically induced by PD1, including BATF or IL10 which have previously been linked to PD1 activity. Together with the work of others this confirms that PD1 is the sole effector of T cell exhaustion and that infection is responsible for BATF and IL10 up regulation. As a consequence future therapeutic strategies will be confined to the inhibition of PD1 and not a downstream effector.

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