ArticleJournal of leukocyte biology2022
T cell activation and IFNγ modulate organ dysfunction in LPS-mediated inflammation.
Article in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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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
8 citing papers in PubMed, 16 citations in OpenAlex.
- T-Cell Memory Affects Lung Responses to Cecal Ligation and Puncture.Shock (Augusta, Ga.) · 2026Article
- IL17FMolecular medicine (Cambridge, Mass.) · 2026Article
- Loss of M1 Acetylcholine Receptor-mediated Orexinergic Activity Contributes to Immune Dysfunction in Experimental Sepsis.Research square · 2025Article
- CD38 promotes LPS-induced innate-like activation and proliferation of CD8Frontiers in aging · 2025Article
- M1 cholinergic signaling in the brain modulates cytokine levels and splenic cell sub-phenotypes following cecal ligation and puncture.Molecular medicine (Cambridge, Mass.) · 2024Article
- Identification of immune infiltration and cuproptosis-related molecular clusters in tuberculosis.Frontiers in immunology · 2023Article
- Angiotensin II enhances bacterial clearance via myeloid signaling in a murine sepsis model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- T-Cell Activation and LPS: A Dangerous Duo for Organ Dysfunction.Journal of leukocyte biology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
LPS challenge is used to model inflammation-induced organ dysfunction. The effects of T cell activation on LPS-mediated organ dysfunction and immune responses are unknown. We studied these interactions through in vivo administration of anti-CD3ε (CD3) T cell activating antibody and LPS. Mortality in response to high-dose LPS (LPSHi; 600 μg) was 60%; similar mortality was observed with a 10-fold reduction in LPS dose (LPSLo; 60 μg) when administered with CD3 (CD3LPSLo). LPSHi and CD3LPSLo cohorts suffered severe organ dysfunction. CD3LPSLo led to increased IFNγ and IL12p70 produced by T cells and dendritic cells (cDCs) respectively. CD3LPSLo caused cDC expression of CD40 and MHCII and prevented PD1 expression in response to CD3. These interactions led to the generation of CD4 and CD8 cytolytic T cells. CD3LPSLo responded to IFNγ or IL12p40 blockade, in contrast to LPSHi. The combination of TCR activation and LPS (CD3LPSLo) dysregulated T cell activation and increased LPS-associated organ dysfunction and mortality through T cell and cDC interactions.
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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.