ArticleInflammatory bowel diseases2013
Lineage targeted MHC-II transgenic mice demonstrate the role of dendritic cells in bacterial-driven colitis.
Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Studying the cellular basis of small bowel enteropathy using high-parameter flow cytometry in mouse models of primary antibody deficiency.Frontiers in immunology · 2024Article
- Epithelial-myeloid exchange of MHC class II constrains immunity and microbiota composition.Cell reports · 2021Article
- Genetic and commensal induction of IL-18 drive intestinal epithelial MHCII via IFNγ.Mucosal immunology · 2021Article
- Why do intestinal epithelial cells express MHC class II?Immunology · 2021Review
- Intestinal Epithelial Expression of MHCII Determines Severity of Chemical, T-Cell-Induced, and Infectious Colitis in Mice.Gastroenterology · 2020Article
- Lack of Effect of Murine Norovirus Infection on the CD4Comparative medicine · 2020Article
- Smad nuclear interacting protein 1 (SNIP1) inhibits intestinal inflammation through regulation of epithelial barrier function.Mucosal immunology · 2018Article
- Epithelial MHC Class II Expression and Its Role in Antigen Presentation in the Gastrointestinal and Respiratory Tracts.Frontiers in immunology · 2018Review
- Primary cultures of mouse small intestinal epithelial cells using the dissociating enzyme type I collagenase and hyaluronidase.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Atypical MHC class II-expressing antigen-presenting cells: can anything replace a dendritic cell?Nature reviews. Immunology · 2014Review
- Interferon-γ induces expression of MHC class II on intestinal epithelial cells and protects mice from colitis.PloS one · 2014Article
- Systemic macrophage depletion inhibits Helicobacter bilis-induced proinflammatory cytokine-mediated typhlocolitis and impairs bacterial colonization dynamics in a BALB/c Rag2-/- mouse model of inflammatory bowel disease.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundInflammatory bowel disease (IBD) pathogenesis involves an inadequately controlled immune reaction to intestinal microbiota, and CD4(+) T cells, dependent on MHC class II (MHC-II) processing and presentation by antigen-presenting cells (APC), play important roles. The role of professional APC (macrophages and dendritic cells [DCs]) and nonprofessional APC (intestinal epithelial cells [IECs]) in microbial-driven intestinal inflammation remains controversial.
methodsWe generated transgenic animals on an MHC-II(-/-) genetic background in which MHC-II is expressed on 1) DC via the CD11c promoter (CD11cTg) or 2) IEC via the fatty acid binding protein (liver) promoter (EpithTg). These mice were crossed with Rag2(-/-) mice to eliminate T and B cells (CD11cTg/Rag2(-/-) and EpithTg/Rag2(-/-)). Helicobacter bilis (Hb) infection and adoptive transfer (AT) of naïve CD4 T cells were used to trigger IBD.
resultsCD11cTg/Rag2(-/-) mice infected with Hb+AT developed severe colitis within 3 weeks post-AT, similar to disease in positive control Rag2(-/-) mice infected with Hb+AT. CD11cTg/Rag2(-/-) mice given AT alone or Hb alone had significantly less severe colitis. In contrast, EpithTg/Rag2(-/-) mice infected with Hb+AT developed mild colitis by 3 weeks and even after 16 weeks post-AT had only mild lesions.
conclusionsMHC-II expression restricted to DCs is sufficient to induce severe colitis in the presence of T cells and a microorganism such as Hb within 3 weeks of AT. Expression of MHC-II solely on IEC in the presence of a microbial trigger and T cells was insufficient to trigger severe colitis.
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