ArticleAllergology international : official journal of the Japanese Society of Allergology2016
TIM-3 is not essential for development of airway inflammation induced by house dust mite antigens.
Article in Allergology international : official journal of the Japanese Society of Allergology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Tim-3 is dispensable for allergic inflammation and respiratory tolerance in experimental asthma.PloS one · 2021Article
- IL-33, IL-25 and TSLP contribute to development of fungal-associated protease-induced innate-type airway inflammation.Scientific reports · 2018Article
- TIM4-TIM1 interaction modulates Th2 pattern inflammation through enhancing SIRT1 expression.International journal of molecular medicine · 2017Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundT cell immunoglobulin domain and mucin domain-containing molecule 3 (TIM-3), which is preferentially expressed on Th1 cells rather than Th2 cells, is considered to be a negative regulator of Th1 cell function. This suggests that TIM-3 indirectly enhances Th2-type immune responses by suppressing Th1 cell function.
methodsTo investigate TIM-3's possible involvement in Th2-type acute and chronic airway inflammation, wild-type and TIM-3-deficient (TIM-3
resultsDespite constitutive expression of TIM-3 mRNA in the lungs, the number of eosinophils in bronchoalveolar lavage fluids (BALFs) and the score of pulmonary inflammation were comparable between wild-type and TIM-3
conclusionsOur findings indicate that, in mice, TIM-3 is not essential for development of HDM-induced acute or chronic allergic airway inflammation, although it appears to be involved in reduced lymphocyte recruitment during HDM-induced chronic allergic airway inflammation.
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Registered trials
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