Extricating human tumour immune alterations from tissue inflammation

免疫系统 炎症 生物 免疫学 电池类型 抗原 癌症研究 细胞 遗传学
作者
Florian Mair,Jami R. Erickson,Marie Frutoso,A Konecny,Evan Greene,Valentin Voillet,Nicholas J. Maurice,Anthony Rongvaux,Douglas R. Dixon,Brittany Barber,Raphaël Gottardo,Martin Prlic
出处
期刊:Nature [Springer Nature]
卷期号:605 (7911): 728-735 被引量:92
标识
DOI:10.1038/s41586-022-04718-w
摘要

Abstract Immunotherapies have achieved remarkable successes in the treatment of cancer, but major challenges remain 1,2 . An inherent weakness of current treatment approaches is that therapeutically targeted pathways are not restricted to tumours, but are also found in other tissue microenvironments, complicating treatment 3,4 . Despite great efforts to define inflammatory processes in the tumour microenvironment, the understanding of tumour-unique immune alterations is limited by a knowledge gap regarding the immune cell populations in inflamed human tissues. Here, in an effort to identify such tumour-enriched immune alterations, we used complementary single-cell analysis approaches to interrogate the immune infiltrate in human head and neck squamous cell carcinomas and site-matched non-malignant, inflamed tissues. Our analysis revealed a large overlap in the composition and phenotype of immune cells in tumour and inflamed tissues. Computational analysis identified tumour-enriched immune cell interactions, one of which yields a large population of regulatory T (T reg ) cells that is highly enriched in the tumour and uniquely identified among all haematopoietically-derived cells in blood and tissue by co-expression of ICOS and IL-1 receptor type 1 (IL1R1). We provide evidence that these intratumoural IL1R1 + T reg cells had responded to antigen recently and demonstrate that they are clonally expanded with superior suppressive function compared with IL1R1 − T reg cells. In addition to identifying extensive immunological congruence between inflamed tissues and tumours as well as tumour-specific changes with direct disease relevance, our work also provides a blueprint for extricating disease-specific changes from general inflammation-associated patterns.
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