ArticleCell reports2014
Tissue-expressed B7-H1 critically controls intestinal inflammation.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 63 citations in OpenAlex.
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- Adaptive immune resistance at the tumour site: mechanisms and therapeutic opportunities.Nature reviews. Drug discovery · 2022Review
- The immune checkpoint B7-H3 (CD276) regulates adipocyte progenitor metabolism and obesity development.Science advances · 2022Article
- Fibroblast-like cells Promote Wound Healing via PD-L1-mediated Inflammation Resolution.International journal of biological sciences · 2022Article
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- PD-1 restraint of regulatory T cell suppressive activity is critical for immune tolerance.The Journal of experimental medicine · 2021Article
- The Enhanced Inhibitory Effect of Estrogen on PD-L1 Expression Following Nrf2 Deficiency in the AOM/DSS Model of Colitis-Associated Cancer.Frontiers in oncology · 2021Article
- Inhibition of PD-1 Protects against TNBS-Induced Colitis via Alteration of Enteric Microbiota.BioMed research international · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
B7-H1 (PD-L1) on immune cells plays an important role in T cell coinhibition by binding its receptor PD-1. Here, we show that both human and mouse intestinal epithelium express B7-H1 and that B7-H1-deficient mice are highly susceptible to dextran sodium sulfate (DSS)- or trinitrobenzenesulfonic acid (TNBS)-induced gut injury. B7-H1 deficiency during intestinal inflammation leads to high mortality and morbidity, which are associated with severe pathological manifestations in the colon, including loss of epithelial integrity and overgrowth of commensal bacteria. Results from bone marrow chimeric and knockout mice show that B7-H1 expressed on intestinal parenchyma, but not on hematopoietic cells, controls intestinal inflammation in an adaptive immunity-independent fashion. Finally, we demonstrate that B7-H1 dampened intestinal inflammation by inhibiting tumor necrosis factor α (TNF-α) production and by stimulating interleukin 22 secretion from CD11c(+)CD11b(+) lamina propria cells. Thus, our data uncover a mechanism through which intestinal tissue-expressed B7-H1 functions as an essential ligand for innate immune cells to prevent gut inflammation.
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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.