ArticleMediators of inflammation2015
Differential Contribution of BLT1 and BLT2 to Leukotriene B4-Induced Human NK Cell Cytotoxicity and Migration.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Immunoregulatory mechanisms of the arachidonic acid pathway in cancer.FEBS letters · 2025Review
- Metabolomic Effects of Folic Acid Supplementation in Adults: Evidence from the FACT Trial.The Journal of nutrition · 2024Article
- Two distinct forms of human BLT2: long-form and short-form BLT2.Frontiers in cell and developmental biology · 2023Review
- The role of human mast cells in allergy and asthma.Bioengineered · 2022Review
- Receptors for pro-resolving mediators are increased in Alzheimer's disease brain.Brain pathology (Zurich, Switzerland) · 2020Article
- Eicosanoid and Specialized Proresolving Mediator Regulation of Lymphoid Cells.Trends in biochemical sciences · 2019Review
- Pharmacogenomics of Prostaglandin and Leukotriene Receptors.Frontiers in pharmacology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Accumulating evidence indicates that leukotriene B4 (LTB4) via its receptors BLT1 and/or BLT2 (BLTRs) could have an important role in regulating infection, tumour progression, inflammation, and autoimmune diseases. In the present study, we showed that LTB4 not only augments cytotoxicity by NK cells but also induces their migration. We found that approximately 30% of fresh NK cells express BLT1, 36% express BLT2, and 15% coexpress both receptors. The use of selective BLTR antagonists indicated that BLT1 was involved in both LTB4-induced migration and cytotoxicity, whereas BLT2 was involved exclusively in NK cell migration, but only in response to higher concentrations of LTB4. BLT1 and BLT2 expression increased after activation of NK cells with IL-2 and IL-15. These changes of BLTR expression by cytokines were reflected in enhanced NK cell responses to LTB4. Our findings suggest that BLT1 and BLT2 play differential roles in LTB4-induced modulation of NK cell activity.
Indexed as
Identifiers
What OpenQuestion holds
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.