Evidence map›Paper›PMID 36633583›Full record

ArticleCancer immunology research2023

CD161 Characterizes an Inflamed Subset of Cytotoxic T Lymphocytes Associated with Prolonged Survival in Human Papillomavirus-Driven Oropharyngeal Cancer.

Ye Wei, Tingting Xu, Chong Li, Xin Zhou, Wei Qian, Chunying Shen, Qifeng Wang, Xing Xing, Xiaomin Ou, Xiayun He and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cancer immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 17 citations in OpenAlex.

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  12. Immune profiling identifies CD161Journal of translational medicine · 2025
    Article
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  16. Review
  17. Journal of thoracic disease · 2024
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  19. Poor clinical outcomes and immunoevasive contexture in CD161Journal for immunotherapy of cancer · 2024
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Ye Wei *Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-3804-2447
Tingting Xu *Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-5920-808X
Chong Li *Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-7988-3069
Xin Zhou *Department of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-7184-1101
Wei QianDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-1536-745X
Chunying ShenDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-1286-4354
Qifeng WangDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-0564-6076
Xing XingDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-8470-3624
Xiaomin OuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-9162-1950
Xiayun HeDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-1652-3012
Hongmei YinDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0003-2642-3135
Chaosu HuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-6407-3311
Yu WangDepartment of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-6712-2879
Qinghai JiDepartment of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0002-3412-009X
Fengtao SuCancer Institute, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0003-1836-4606
Xueguan LuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai Medical College of Fudan University, Shanghai, China.ORCID 0000-0001-9829-3312
Fudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papillomavirus (HPV)-driven oropharyngeal carcinoma (OPSCC) is distinct from tobacco- or alcohol-associated OPSCC and has a unique immune landscape. Studies have supported the heterogeneity of T cells, accompanied by a broad repertoire of T-cell responses, within tumors driven by HPV infection. However, the phenotype and function of these HPV-related T cells remain unclear. Using a combination of single-cell RNA sequencing, flow cytometry, pharmacologic inhibition, and immunofluorescence staining, we explored the prognostic implication of HPV-related T cells and further validated our findings in two independent cohorts. Cytotoxic T lymphocytes (CTL) within OPSCC displayed a spectrum of transcriptional signatures. Among which, we identified CD161 receptor, encoded by KLRB1, as a potential marker to distinguish the CTL subsets in HPV-positive OPSCC with a divergent evolutionary trajectory. In-depth analysis revealed that CD161+ CTLs exhibited a more robust immune response over the CD161- counterparts and a T cell-inflamed phenotype that could be further reinvigorated by immune-checkpoint blockade. Despite the high expression of exhaustion markers, reinforcement of CD161+ CTL reactivity was expected to boost immune responses, considering their functional reversibility. We further confirmed that the high level of intratumoral CD161+ CTLs associated with a favorable treatment response and prolonged overall survival. Therefore, our research not only provides an insight into the immune landscape of HPV-driven OPSCC but also sheds light on a special subset of CTLs with prognostic and therapeutic significance.

Indexed as

Carcinoma, Squamous CellOropharyngeal NeoplasmsPapillomavirus InfectionsHuman Papillomavirus VirusesHumansNK Cell Lectin-Like Receptor Subfamily BPrognosisT-Lymphocytes, CytotoxicKLRB1 protein, humanNK Cell Lectin-Like Receptor Subfamily B

Identifiers

PMID36633583
PMCPMC9975669
OpenAlexW4315705066

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.