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γδ T cells are effectors of immunotherapy in cancers with HLA class I defects

ABSTRACT: γδ T cells are effectors of immunotherapy in cancers with HLA class I defects

PROVIDER: PRJNA894171 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22031356_1.fastq.gz	Fastqsanger.gz
	SRR22031356_2.fastq.gz	Fastqsanger.gz
	SRR22031357_1.fastq.gz	Fastqsanger.gz
	SRR22031357_2.fastq.gz	Fastqsanger.gz

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γδ T cells are effectors of immunotherapy in cancers with HLA class I defects

Project description:DNA mismatch repair deficient (MMR-d) cancers present an abundance of neoantigens that likely underlies their exceptional responsiveness to immune checkpoint blockade (ICB). However, MMR-d colon cancers that evade CD8+ T cells through loss of Human Leukocyte Antigen (HLA) class I-mediated antigen presentation frequently remain responsive to ICB, suggesting the involvement of other immune effector cells.

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γδ T cells are effectors of immunotherapy in cancers with HLA class I defects.

Project description:DNA mismatch repair-deficient (MMR-d) cancers present an abundance of neoantigens that is thought to explain their exceptional responsiveness to immune checkpoint blockade (ICB)1,2. Here, in contrast to other cancer types3-5, we observed that 20 out of 21 (95%) MMR-d cancers with genomic inactivation of β2-microglobulin (encoded by B2M) retained responsiveness to ICB, suggesting the involvement of immune effector cells other than CD8+ T cells in this context. We next identified a strong association between B2M inactivation and increased infiltration by γδ T cells in MMR-d cancers. These γδ T cells mainly comprised the Vδ1 and Vδ3 subsets, and expressed high levels of PD-1, other activation markers, including cytotoxic molecules, and a broad repertoire of killer-cell immunoglobulin-like receptors. In vitro, PD-1+ γδ T cells that were isolated from MMR-d colon cancers exhibited enhanced reactivity to human leukocyte antigen (HLA)-class-I-negative MMR-d colon cancer cell lines and B2M-knockout patient-derived tumour organoids compared with antigen-presentation-proficient cells. By comparing paired tumour samples from patients with MMR-d colon cancer that were obtained before and after dual PD-1 and CTLA-4 blockade, we found that immune checkpoint blockade substantially increased the frequency of γδ T cells in B2M-deficient cancers. Taken together, these data indicate that γδ T cells contribute to the response to immune checkpoint blockade in patients with HLA-class-I-negative MMR-d colon cancers, and underline the potential of γδ T cells in cancer immunotherapy.

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HLA Class I submissions 240531

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