ArticleJournal of immunology (Baltimore, Md. : 1950)2010
T cell pathways involving CTLA4 contribute to a model of acute lung injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Plasma glutamate-modulated interaction of A2AR and mGluR5 on BMDCs aggravates traumatic brain injury-induced acute lung injury.The Journal of experimental medicine · 2013Trial
- Association of peripheral blood lymphocytes and immunoglobulins with disease severity in pediatric acute respiratory distress syndrome: an age-stratified retrospective study.BMC pediatrics · 2026Article
- Prolonged early-life antibiotic exposure alters gut microbiota but does not exacerbate lung injury in a rat pup model.Pediatric research · 2025Article
- Gut-derived immune cells and the gut-lung axis in ARDS.Critical care (London, England) · 2024Review
- Bacterial sepsis triggers stronger transcriptomic immune responses in larger primates.Proceedings. Biological sciences · 2024Article
- Observational
- Acute inflammation alters lung lymphocytes and potentiates innate-like behavior in young mouse lung CD8 T cells, resembling lung CD8 T cells from old mice.Journal of leukocyte biology · 2023Article
- Lung injury induces a polarized immune response by self-antigen-specific CD4Cell reports · 2023Article
- Corticosteroids treatment for pediatric acute respiratory syndrome: A critical review.Saudi medical journal · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Time‑dependent changes in NLRP3 and Nrf2 levels in lipopolysaccharide‑induced acute lung injury.International journal of molecular medicine · 2022Article
- Acute stress induces an inflammation dominated by innate immunity represented by neutrophils in mice.Frontiers in immunology · 2022Article
- Immunotherapy strategies and prospects for acute lung injury: Focus on immune cells and cytokines.Frontiers in pharmacology · 2022Review
- Potential therapeutics in pediatric acute respiratory distress syndrome: what does the immune system have to offer? A narrative review.Translational pediatrics · 2021Review
- Machine Learning-Based Discovery of a Gene Expression Signature in Pediatric Acute Respiratory Distress Syndrome.Critical care explorations · 2021Article
- Cell-Type-Specific Immune Dysregulation in Severely Ill COVID-19 Patients.Cell reports · 2021Article
- Insights into pathogenesis of fatal COVID-19 pneumonia from histopathology with immunohistochemical and viral RNA studies.Histopathology · 2020Article
- Cell type-specific immune dysregulation in severely ill COVID-19 patients.medRxiv : the preprint server for health sciences · 2020Article
- Article
- The novel immunomodulatory biologic LMWF5A for pharmacological attenuation of the "cytokine storm" in COVID-19 patients: a hypothesis.Patient safety in surgery · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Acute lung injury (ALI) is a frequent pulmonary complication in critically ill patients. We characterized a murine model of LPS-induced ALI, focusing on Th cells. Following LPS administration, bronchoalveolar lavage lymphocytes, neutrophils, IL-6, TNF-alpha, and albumin were increased. Analysis of LPS-induced T cells revealed increased Th cell-associated cytokines (IL-17A, -17F, and -22), as well as increased expression of CD69 (a cell activation marker), Foxp3, and CTLA4 in CD4(+) T cells. Administration of anti-CTLA4 Ab decreased LPS-induced bronchoalveolar lavage albumin and IL-17A, while increasing CD4(+)Foxp3(+) cell number and Foxp3 expression in CD4(+)Foxp3(+) cells. These data suggest that pulmonary LPS administration promotes CD4(+) T cells and that T cell pathways involving CTLA4 contribute to ALI.
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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.