ArticlePloS one2017
Increased PD-1 Expression and Altered T Cell Repertoire Diversity Predict Mortality in Patients with Septic Shock: A Preliminary Study.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Pooled prevalence of lymphopenia in all-cause hospitalisations and association with infection: a systematic review and meta-analysis.BMC infectious diseases · 2023Pooled it
- Inhibitory Immune Checkpoint Molecule Expression in Clinical Sepsis Studies: A Systematic Review.Critical care medicine · 2020Pooled it
- Restricted TCR Diversity and Expansion of CD177MedComm · 2026Article
- A whole-blood cryopreservation method streamlines clinical sample collection for multimodal single-cell immune profiling in sepsis.JCI insight · 2026Article
- Immunology of Sepsis.Clinics in chest medicine · 2026Review
- Early biomarkers for predicting sepsis-induced shock: insights from inflammatory pathways and immune response.Frontiers in pharmacology · 2026Review
- Prognostic Nutritional Index as a Novel Biomarker for Predicting Prognosis in Sepsis-Associated Encephalopathy: A Multicenter Retrospective Cohort Study.Emergency medicine international · 2026Article
- Predictive value of PD-1Scientific reports · 2025Article
- Risk Factors for Cytomegalovirus Reactivation and Its Impact on Clinical Outcomes in Immunocompetent Seropositive Patients Admitted to the Intensive Care Unit: A Single-Center Prospective Observational Study.Infectious diseases & clinical microbiology · 2025Article
- The accumulation of myeloid-derived suppressor cells participates in abdominal infection-induced tumor progression through the PD-L1/PD-1 axis.Molecular oncology · 2025Article
- Insights into sepsis-induced apoptosis: Interplay between programmed cell death and interleukin-7.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2025Review
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- The Changes in the Quantity of Lymphocyte Subpopulations during the Process of Sepsis.International journal of molecular sciences · 2024Review
- Peripheral PD-1Frontiers in immunology · 2024Observational
- The Role of Mesenchymal Stem Cell Secretome in the Inflammatory Mediators and the Survival Rate of Rat Model of Sepsis.Biomedicines · 2023Article
- The implication of targeting PD-1:PD-L1 pathway in treating sepsis through immunostimulatory and anti-inflammatory pathways.Frontiers in immunology · 2023Review
- Immune Checkpoint Receptors Signaling in T Cells.International journal of molecular sciences · 2022Review
- Immune Modulation and Cytomegalovirus Reactivation in Sepsis-induced Immunosuppression: A Pilot Study.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2022Article
- Beneficial Immune Regulation by Biological Response Modifier Glucans in COVID-19 and Their Envisaged Potentials in the Management of Sepsis.Frontiers in immunology · 2022Review
- Limited TCR repertoire andiScience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis causes impairment of innate and adaptive immunity by multiple mechanisms, including depletion of immune effector cells and T cell exhaustion. Although lymphocyte dysfunction is associated with increased mortality and potential reactivation of latent viral infection in patients with septic shock, the relation between viral reactivation and lymphocyte dysfunction is obscure. The objectives of this study were 1) to determine the relation of lymphocyte dysfunction to viral reactivation and mortality, and 2) to evaluate recovery of lymphocyte function during septic shock, including T cell receptor (TCR) diversity and the expression of programmed death 1 (PD-1). In 18 patients with septic shock and latent cytomegalovirus (CMV) infection, serial blood samples were obtained on days 1, 3, and 7 after the onset of shock, and immune cell subsets and receptor expression were characterized by flow cytometry. TCR diversity of peripheral blood mononuclear cells was analyzed by Multi-N-plex PCR, and CMV DNA was quantified using a real-time PCR kit. A decrease of TCR diversity and monocyte HLA-DR expression were observed in the early stage of septic shock, while CD4+ T cells displayed an increase of PD-1 expression. Significant lymphopenia persisted for at least 7 days following the onset of septic shock. Normalization of TCR diversity and PD-1 expression was observed by day 7, except in patients who died. CMV reactivation was detected in 3 of the 18 patients during the first week of their ICU stay and all 3 patients died. These changes are consistent with the early stage of immune cell exhaustion and indicate the importance of normal lymphocyte function for recovery from septic shock. Ongoing lymphocyte dysfunction is associated with CMV reactivation and dissemination, as well as with unfavorable outcomes.
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Registered trials
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.