Increased cycles of DC/CIK immunotherapy decreases frequency of Tregs in patients with resected NSCLC

Song, Hao; Liu, Shujuan; Zhao, Zhen; Sun, Weihong; Wei, Xiaofang; Ma, Xuexiao; Zhao, Peng; Gao, Daiqing

doi:10.1016/j.intimp.2017.09.014

Cited by 21 publications

(15 citation statements)

References 43 publications

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“…Moreover, they have also shown that the maturation rate of DCs in patients with lung cancer is independently associated with survival [97, 98]. The ratio of Tregs and cancer recurrence decreases after DC vaccination combined with cytokine-induced killer (DC/CIK) immunotherapy in patients with NSCLC, indicating that this strategy is generally successful [99]. MoDCs are most widely used due to their easy acquisition from patients [100].…”

Section: Progress In the Clinical Application Of DC Function Restorationmentioning

confidence: 99%

Impaired dendritic cell functions in lung cancer: a review of recent advances and future perspectives

Wang

Huang

2019

Cancer Communications

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Lung cancer is the leading cause of cancer mortality worldwide. Dendritic cells (DCs) are the key factors providing protective immunity against lung tumors and clinical trials have proven that DC function is reduced in lung cancer patients. It is evident that the immunoregulatory network may play a key role in the failure of the immune response to terminate tumors. Lung tumors likely employ numerous strategies to suppress DC-based anti-tumor immunity. Here, we summarize the recent advances in our understanding on lung tumor-induced immunosuppression in DCs, which affects the initiation and development of T-cell responses. We also describe which existing measures to restore DC function may be useful for clinical treatment of lung tumors. Furthering our knowledge of how lung cancer cells alter DC function to generate a tumor-supportive environment will be essential in order to guide the design of new immunotherapy strategies for clinical use.

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Section: Progress In the Clinical Application Of DC Function Restorationmentioning

confidence: 99%

Impaired dendritic cell functions in lung cancer: a review of recent advances and future perspectives

Wang

Huang

2019

Cancer Communications

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“…Microglia are activated soon after cerebral ischemia/reperfusion injury and are the main cells that cause serious inflammation ( 22 , 23 ). Iba 1 is a protein that is specifically expressed on microglia ( 24 , 25 ).…”

Section: Resultsmentioning

confidence: 99%

Lack of sphingomyelin synthase 2 reduces cerebral ischemia/reperfusion injury by inhibiting microglial inflammation in mice

Yu¹,

Hu²,

Yang³

et al. 2020

Exp Ther Med

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Recanalization of blood flow after ischemia can lead to ischemia/reperfusion injury, and inflammation plays an important role in the mechanisms behind cerebral ischemia/reperfusion injury. Sphingomyelin synthase 2 (SMS2) deficiency reduces inflammation; however, the effect and mechanism of action of SMS2 on the inflammatory response after cerebral ischemia/reperfusion injury are still unclear. Wild-type (WT) and SMS2 knockout C57BL/6 mice were used to establish a model of cerebral ischemia/reperfusion. The neurological deficit score was evaluated with Longa's method, and infarct volume was evaluated by magnetic resonance imaging and 2,3,5-triphenyltetrazolium chloride staining. Neurological deficit and infarct volume were used to evaluate the degree of cerebral ischemia/reperfusion injury in mice. Western blotting, reverse transcription-quantitative PCR and immunofluorescence were used to detect the expression profiles. The neurological deficit score of SMS2-/mice was significantly lower than that of WT mice at 72 h after cerebral ischemia/reperfusion injury (P= 0.027), but not significantly different at 24 h (P=0.064). Compared with WT mice at 24 and 72 h after cerebral ischemia/reperfusion, the infarct volume of SMS2-/mice was decreased, the expression of pro-inflammatory cytokines galectin 3 and interleukin-1β were decreased, the activation of microglia was decreased, and the nuclear translocation of NF-κB p65 was decreased, but the expression of the anti-inflammatory factor arginase 1 was increased. Lack of SMS2 in mice can help to reduce the inflammatory reaction by inhibiting the activation of NF-κB signaling pathway, further attenuating cerebral ischemia/reperfusion injury in mice.

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“…These results are consistent with previous research. Tregs constitutively express the intracellular transcription factor Foxp3 [31]. We found that the expression of Foxp3 was increased in tumor tissues and CD200R inhibitor decreased the level of Foxp3.…”

Section: Discussionmentioning

confidence: 99%

Role of CD200/CD200R Signaling Pathway in Regulation of CD4+T Cell Subsets During Thermal Ablation of Hepatocellular Carcinoma

et al. 2019

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BackgroundIn this study, we assessed the role of CD200 and CD200 receptor (CD200R) in regulating CD4+T cell subsets and assessed the therapeutic efficacy of thermal ablation for liver hepatocellular carcinoma (HCC) in rats.Material/MethodsSeventy-eight male C57BL/6 rats were randomly divided into 7 groups: a control group, a model group, a CD200FC group, an anti-CD200R1 mAb group, a thermal ablation group, a thermal ablation+CD200 FC group, and a thermal ablation+anti-CD200R1 mAb group. The levels of CD200, CD200R1, Th1, Th17, and Treg in peripheral blood were detected by flow cytometry. Immunohistochemistry was used to detect CD200, CD200R1, IFN-γ, IL-17, Foxp3 protein expression in tumor tissues.ResultsThe levels of CD200, CD200R1, Th17, and Treg were significantly increased after CD200FC treatment (p<0.05). After treatment with anti-CD200R1 mAb, the levels of CD200, CD200R1, Th17, and Treg decreased and Th1 increased. Compared with the control group, the expression of CD200, CD200R1, IL-17, and Foxp3 in the model group increased significantly, and the expression of IFN-γ decreased significantly (p<0.05). The expression of CD200, CD200R1, IL-17, and Foxp3 was significantly reduced by adding anti-CD200R1 mAb, and the expression of IFN-γ was increased (p<0.05). After the thermal ablation treatment, the proteins continued to decrease and the expression of IFN-γ continued to increase.ConclusionsThe CD200/CD200R pathway participates in HCC tumor growth and the expression of CD4+T cell subsets in cancer tissues. Furthermore, thermal ablation treatment inhibited cancer recurrence.

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Increased cycles of DC/CIK immunotherapy decreases frequency of Tregs in patients with resected NSCLC

Cited by 21 publications

References 43 publications

Impaired dendritic cell functions in lung cancer: a review of recent advances and future perspectives

Impaired dendritic cell functions in lung cancer: a review of recent advances and future perspectives

Lack of sphingomyelin synthase 2 reduces cerebral ischemia/reperfusion injury by inhibiting microglial inflammation in mice

Role of CD200/CD200R Signaling Pathway in Regulation of CD4+T Cell Subsets During Thermal Ablation of Hepatocellular Carcinoma

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