Evidence map›Paper›PMID 28673007›Full record

ArticleExperimental and therapeutic medicine2017

Cytokine-induced killer cell therapy for modulating regulatory T cells in patients with non-small cell lung cancer.

Baodan Yu, Junli Wang, Chen He, Wei Wang, Jianli Tang, Runhui Zheng, Chengzhi Zhou, Huanhuan Zhang, Zhiping Fu, Qiasheng Li and 1 more

Abstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

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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

11 authors.

Baodan YuDepartment of Clinical Laboratory, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120, P.R. China.
Junli WangDepartment of Respiration, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong 518100, P.R. China.
Chen HeDepartment of Respiratory Medicine, The Affiliated Shenzhen Bao'an Hospital of Southern Medical University, Shenzhen, Guangdong 518101, P.R. China.
Wei WangDepartment of Medical Oncology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010050, P.R. China.
Jianli TangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Runhui ZhengDepartment of Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510120, P.R. China.
Chengzhi ZhouState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Huanhuan ZhangState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Zhiping FuDepartment of Respiratory Medicine, Jingzhou Central Hospital, The Second Clinical Medical College, Yangtze University, Jingzhou, Hubei 434020, P.R. China.
Qiasheng LiState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.
Jun XuState Key Laboratory of Respiratory Diseases, Guangzhou Institute of Respiratory Diseases, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have reported that regulatory T cells (Tregs), which are physiologically engaged in the maintenance of immunological self-tolerance, have a critical role in the regulation of the antitumor immune response. Targeting Tregs has the potential to augment cancer vaccine approaches. The current study therefore aimed to evaluate the role of cytokine-induced killer (CIK) cell infusion in modulating Tregs in patients with non-small cell lung cancer (NSCLC). A total of 15 patients with advanced NSCLC were treated by an infusion of CIK cells derived from autologous peripheral blood mononuclear cells (PBMCs). By using flow cytometry and liquid chip analysis, subsets of T cells and natural killer (NK) cells in peripheral blood, and plasma cytokine profiles in the treated patients, were analyzed at 2 and 4 weeks after CIK cell infusion. Cytotoxicity of PBMCs (n=15) and NK cells (n=6) isolated from NSCLC patients was evaluated before and after CIK cell therapy. Progression-free survival (PFS) and overall survival (OS) were also assessed. Analysis of the immune cell populations before and after treatment showed a significant increase in NK cells (P<0.05) concomitant with a significant decrease in Tregs (P<0.01) at 2 weeks post-infusion of CIK cells compared with the baseline. NK group 2D receptor (NKG2D) expression on NK cells was also significantly increased at 2 weeks post-infusion compared with the baseline (P<0.05). There was a positive correlation between NKG2D expression and the infusion number of CIK cells (P<0.05). When evaluated at 2 weeks after CIK cell therapy, the cytotoxicity of PBMCs and isolated NK cells was significantly increased compared with the baseline (P<0.01 and P<0.05). Correspondingly, plasma cytokine profiles showed significant enhancement of the following antitumor cytokines: Interferon (IFN)-γ (P<0.05), IFN-γ-inducible protein 10 (P<0.01), tumor necrosis factor-α (P<0.001), granulocyte-macrophage colony-stimulating factor (P<0.01), monocyte chemotactic protein-3 (P<0.01) and interleukin-21 (P<0.05) at 2 weeks post-infusion, compared with the baseline. At the same time, the expression of transforming growth factor-β1, which is primarily produced by Tregs, was significantly decreased compared with the baseline (P<0.05). Median PFS and OS in the CIK cell treatment group were significantly increased compared with the control group (PFS, 9.98 vs. 5.44 months, P=0.038; OS, 24.17 vs. 20.19 months, P=0.048). No severe side-effects were observed during the treatment period. In conclusion, CIK cell therapy was able to suppress Tregs and enhance the antitumor immunity of NK cells in advanced NSCLC patients. Therefore, CIK cell treatment may improve PFS and OS in patients with advanced NSCLC. CIK cell infusion may have therapeutic value for patients with advanced NSCLC, as a treatment that can be combined with chemotherapy and radiotherapy.

Indexed as

cytokine-induced killer cellsnon-small cell lung cancerregulatory T cells

Identifiers

PMID28673007
PMCPMC5488714

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.