ArticleJournal of gastroenterology2014
Immunoregulatory function of PIR-A/B+ DCs in the inflammatory responses of dextran sodium sulfate-induced colitis.
Article in Journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 5 citations in OpenAlex.
- Induction of PIR-A/BJournal of gastroenterology · 2018Article
- Interleukin(IL)-36α and IL-36γ Induce Proinflammatory Mediators from Human Colonic Subepithelial Myofibroblasts.Frontiers in medicine · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDendritic cells (DCs) may play an important role in forms of inflammatory bowel disease (IBD), such as Crohn's disease and ulcerative colitis. DCs are generally recognized as initiators of acquired immunity and also serve as regulators of both innate and acquired immunity. We used the animal model of colitis induced by dextran sodium sulfate (DSS), and examined whether DCs prepared from the colon show immunoregulatory roles in the termination of DSS-induced colitis.
methodsC57BL/6 mice exposed to DSS for 5 days developed acute colitis. DCs were isolated from the large intestinal lamina propria, and then analyzed for phenotypical, functional, and genetic data.
resultsOnly PIR-A/B(low) conventional DCs (cDCs) were detected in the steady state. However, after the treatment of DSS, PIR-A/B(high) cDCs appeared and gradually increased from day 5 to day 7, at which time the DSS-induced colitis was terminated. Then, allogeneic mixed leukocyte reaction (MLR) was performed. The stimulatory activity of PIR-A/B(high) cDCs obtained on day 7 was very low, and the addition of PIR-A/B(high) cDCs suppressed the T cell proliferation in MLR, indicating the immunoregulatory role of PIR-A/B(high) cDCs. The immunoregulatory role of PIR-A/B(high) cDCs was confirmed by the in vivo transfer experiment, showing their therapeutic effect on DSS-induced colitis. The message level of TGFβi was significantly higher in PIR-A/B(high) cDCs, while that of IFN-γ was highly upregulated in PIR-A/B(low) cDCs, being well in accordance with the fact that PIR-A/B(high) cDCs showed a suppressive function against activated T cells.
conclusionPIR-A/B(high) cDCs showed a suppressive function against activated T cells by producing inhibitory cytokines.
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