scholarly journals Programmed Death-1 Shapes Memory Phenotype CD8 T Cell Subsets in a Cell-Intrinsic Manner

2013 ◽  
Vol 190 (12) ◽  
pp. 6104-6114 ◽  
Author(s):  
Joanna J. Charlton ◽  
Ioannis Chatzidakis ◽  
Debbie Tsoukatou ◽  
Dimitrios T. Boumpas ◽  
George A. Garinis ◽  
...  
2018 ◽  
Author(s):  
Jicheng Hu ◽  
Xiaoqing Chai ◽  
Di Wang ◽  
Shuhua Shu ◽  
Costan Magnussen ◽  
...  

Abstract Background: This study aimed to determine the influence of intraoperative use of non-steroidal anti-inflammatory drugs (NSAIDs) flurbiprofen on postoperative level of programmed death 1 (PD-1) in patients undergoing thoracoscope surgery. Methods: In this prospective double-blind trial, patients were randomized to receive intralipid (Control group, n=34, 0.1ml/kg, i.v.) or flurbiprofen axetil (Flurbiprofen group, n=34, 1mg/kg, i.v.) before the induction of anesthesia and 6 hours after the initial injection. PD-1 level on T-cell subsets, inflammation and immune markers in peripheral blood were examined before induction of anesthesia (T0), and after surgery (24 hours (T1), 72 hours (T2) and 1 week (T3)). A linear mixed model was used to examine whether the changes from baseline values (T0) between groups were different during our study. Results: The increases in the percentages of PD-1(+)CD8(+) T-cell observed at T1 and T2 in the control group were higher than in the flurbiprofen group (T1:12.91%±1.65% versus 7.86%±5.71%, P=0.031; T2:11.54%±1.54% versus 8.75%±1.73%, P=0.004) while no difference was observed at T1 and T2 between the groups in terms of change in percentages of PD-1(+)CD4(+) T-cell. Moreover, extensive changes in the percentages of lymphocytes subsets and the concentrations of inflammatory markers was observed at T1 and T2 after surgery, and flurbiprofen seemed to attenuate the most of changes. Conclusion: Perioperative administration of flurbiprofen attenuated postoperative PD-1 increase on CD8(+) T-cell up to 72 hours, but not after this time. The clinical relevance of changes with PD-1 to long-term outcome of surgery is still unknown. Trial registration: Chinese Clinical Trail Registry, ChiCTR-IPR-15006482 (date of registration June 2015) Keywords: Immune cells; Lung cancer; Flurbiprofen; Programmed death 1.


2016 ◽  
Vol 196 (6) ◽  
pp. 2870-2878 ◽  
Author(s):  
Tatiana M. Garcia-Bates ◽  
Eun Kim ◽  
Fernando Concha-Benavente ◽  
Sumita Trivedi ◽  
Robbie B. Mailliard ◽  
...  

2013 ◽  
Vol 191 (5) ◽  
pp. 2194-2204 ◽  
Author(s):  
Gaëlle Breton ◽  
Nicolas Chomont ◽  
Hiroshi Takata ◽  
Rémi Fromentin ◽  
Jeffrey Ahlers ◽  
...  

2020 ◽  
Vol 8 (2) ◽  
pp. e001593
Author(s):  
Chen Shen ◽  
Qianru Li ◽  
Yongchang Wei ◽  
Yuting Li ◽  
Jun Li ◽  
...  

The COVID-19 outbreak caused by SARS-CoV-2 challenges the medical system by interfering with routine therapies for many patients with chronic diseases. In patients with cancer receiving immune checkpoint inhibitors (ICIs), difficulties also arise from the incomplete understanding of the intricate interplay between their routine treatment and pathogenesis of the novel virus. By referring to previous ICI-based investigations, we speculate that ICIs themselves are not linked to high-infection risks of respiratory diseases or inflammation-related adverse effects in patients with cancer. Moreover, ICI treatment may even enhance coronavirus clearance in some patients with malignant tumor by boosting antiviral T-cell responsiveness. However, the ‘explosive’ inflammation during COVID-19 in some ICI-treated patients with cancer was illustrated as exuberant immunopathological damage or even death. In case of the COVID-19 immunopathogenesis fueled by ICIs, we propose a regular monitor of pathogenic T-cell subsets and their exhaustion marker expression (eg, Th17 and interleukin (IL)-6-producing Th1 subsets with surface programmed death 1 expression) to guide the usage of ICI. Here we aimed to address these considerations, based on available literature and experience from our practice, that may assist with the decision-making of ICI administration during the pandemic.


Blood ◽  
2011 ◽  
Vol 117 (18) ◽  
pp. 4805-4815 ◽  
Author(s):  
Takuya Yamamoto ◽  
David A. Price ◽  
Joseph P. Casazza ◽  
Guido Ferrari ◽  
Martha Nason ◽  
...  

Abstract A highly complex network of coinhibitory and costimulatory receptors regulates the outcome of virus-specific CD8+ T-cell responses. Here, we report on the expression patterns of multiple inhibitory receptors on HIV-specific, cytomegalovirus-specific, and bulk CD8+ T-cell memory populations. In contrast to cytomegalovirus-specific CD8+ T cells, the majority of HIV-specific CD8+ T cells exhibited an immature phenotype and expressed Programmed Death-1, CD160 and 2B4 but not lymphocyte activation gene-3. Notably, before antiretroviral therapy, simultaneous expression of these negative regulators correlated strongly with both HIV load and impaired cytokine production. Suppression of HIV replication by antiretroviral therapy was associated with reduced surface expression of inhibitory molecules on HIV-specific CD8+ T cells. Furthermore, in vitro manipulation of Programmed Death-1 and 2B4 inhibitory pathways increased the proliferative capacity of HIV-specific CD8+ T cells. Thus, multiple coinhibitory receptors can affect the development of HIV-specific CD8+ T-cell responses and, by extension, represent potential targets for new immune-based interventions in HIV-infected persons.


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