ArticleClinical and experimental immunology2011
IL-9(+) IL-10(+) T cells link immediate allergic response to late phase reaction.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Association of variations in theFrontiers in pharmacology · 2023Article
- Recent advances in mechanisms of food allergy and anaphylaxis.F1000Research · 2020Review
- Th9 Cells in Allergic Disease.Current allergy and asthma reports · 2019Review
- Distinct chemokine receptor axes regulate Th9 cell trafficking to allergic and autoimmune inflammatory sites.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- The unique features of Th9 cells and their products.Critical reviews in immunology · 2012Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The mechanism underlying late-phase allergic reactions (LPR) remains incompletely understood. This study aimed to investigate the role of a newly described subset of T cells, interleukin (IL)-9(+) IL-10(+) T cells, in the pathogenesis of LPR. Using a T helper type 2 (Th2) inflammatory mouse model, we examined the frequency of IL-9(+) IL-10(+) T cells in the jejunum by immunohistochemistry. The LPR in the jejunum was observed afterwards. The cytokine profile of IL-9(+) IL-10(+) T cells was characterized and the major cytokine that plays the critical role in the initiation of LPR was investigated. Abundant IL-9(+) IL-10(+) T cells as well as inflammatory cell extravasation in the jejunal sections were observed in sensitized mice 48 h after specific antigen challenge. IL-9(+) IL-10(+) T cells expressed high levels of macrophage inflammatory protein 1 (MIP1) that could be enhanced by T cell receptor activation. MIP1 facilitated macrophage extravasation in local tissue. Macrophage-derived MIP2 contributed to neutrophil infiltration in the intestine in LPR. Pretreatment with anti-MIP antibody inhibited the LPR in the intestine. IL-9(+) IL-10(+) T cells play an important role in LPR. This subset of T cells has the potential to be a novel therapeutic target in the treatment of LPR and LPR-related inflammation.
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Registered trials
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