ArticleShock (Augusta, Ga.)2016
Enhanced Innate Inflammation Induced by Anti-BTLA Antibody in Dual Insult Model of Hemorrhagic Shock/Sepsis.
Article in Shock (Augusta, Ga.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
- Exploring the mechanism of polymorphonuclear neutrophils against sepsis based on immune model.Annals of medicine · 2026Review
- Pirinixic Acid Protects Against Hemorrhagic Shock by Regulating Neutrophil-Associated Key Genes.Shock (Augusta, Ga.) · 2026Article
- Mechanisms of immune suppression in sepsis/shock: one investigator's/lab group's experience (SLB 2024 legacy award presentation).Journal of leukocyte biology · 2025Article
- BTLA contributes to acute-on-chronic liver failure infection and mortality through CD4Nature communications · 2024Article
- [Novel strategy of sepsis immunomodulation targeting dendritic cells].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- PDGFR kinase inhibitor protects against septic death via regulation of BTLA.Science China. Life sciences · 2022Article
- Immunomodulatory Properties of Immune Checkpoint Inhibitors-More than Boosting T-Cell Responses?Cancers · 2022Review
- Sustained elevation of soluble B- and T- lymphocyte attenuator predicts long-term mortality in patients with bacteremia and sepsis.PloS one · 2022Article
- Innate immunity and immunotherapy for hemorrhagic shock.Frontiers in immunology · 2022Review
- The Diagnostic Value of Mitochondrial Mass of Peripheral T Lymphocytes in Early Sepsis.Frontiers in public health · 2022Article
- The Neonatal Innate Immune Response to Sepsis: Checkpoint Proteins as Novel Mediators of This Response and as Possible Therapeutic/Diagnostic Levers.Frontiers in immunology · 2022Review
- Paeonol attenuates inflammation by confining HMGB1 to the nucleus.Journal of cellular and molecular medicine · 2021Article
- Roles of BTLA in Immunity and Immune Disorders.Frontiers in immunology · 2021Review
- The Role of B and T Lymphocyte Attenuator in Respiratory System Diseases.Frontiers in immunology · 2021Review
- Cancer Immunotherapies: From Efficacy to Resistance Mechanisms - Not Only Checkpoint Matters.Frontiers in immunology · 2021Review
- CircC3P1 attenuated pro-inflammatory cytokine production and cell apoptosis in acute lung injury induced by sepsis through modulating miR-21.Journal of cellular and molecular medicine · 2020Article
- Review
- Checkpoint inhibitor therapy in preclinical sepsis models: a systematic review and meta-analysis.Intensive care medicine experimental · 2020Article
- Hyperprogression After Immune-Checkpoint Inhibitor Treatment: Characteristics and Hypotheses.Frontiers in oncology · 2020Review
- Immune Checkpoints: Novel Therapeutic Targets to Attenuate Sepsis-Induced Immunosuppression.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Sepsis following hemorrhagic shock is a common clinical condition, in which innate immune system suffers from severe suppression. B and T lymphocyte attenuator (BTLA) is an immune-regulatory coinhibitory receptor expressed not only on adaptive, but also on innate immune cells. Our previous data showed that BTLA gene deficient mice were protected from septic mortality when compared with wild-type control C57BL/6 mice. Here, we extended our study by treating C57BL/6 mice with an anti-BTLA monoclonal antibody (clone 6A6; reported to have the ability to neutralize or agonize/potentiate BTLA signaling) in a mouse model of hemorrhagic shock (Hem) followed by sepsis induced by cecal ligation and puncture (CLP); positing initially that if BTLA engagement was neutralized, like gene deficiency, an anti-BTLA mAb would have the similar effects on the inflammatory response/morbidity in these mice after such insults. Here, we report that BTLA expression is elevated on innate immune cells after Hem/CLP. However, anti-BTLA antibody treatment increased cytokine (TNF-α, IL-12, IL-10)/chemokine (KC, MIP-2, MCP-1) levels and inflammatory cells (neutrophils, macrophages, dendritic cells) recruitment in the peritoneal cavity, which in turn aggravated organ injury and elevated these animals' mortality in Hem/CLP. When compared with the protective effects of our previous study using BTLA gene deficient mice in a model of lethal septic challenge, we further confirmed BTLA's contribution to enhanced innate cell recruitment, elevated IL-10 levels, and reduced survival, and that engagement of antibody with BTLA potentiates/exacerbates the pathophysiology in Hem/sepsis.
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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 Socratic graph.