ArticleInflammatory bowel diseases2018
CD1a-Expressing Monocytes as Mediators of Inflammation in Ulcerative Colitis.
Article in Inflammatory bowel diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 21 citations in OpenAlex.
- Effects of Notch signaling on the lineage commitment of human peripheral blood monocyte trilineage progenitor under inflammatory conditions.Cell death discovery · 2025Article
- NOD/Scid IL2RγJID innovations : skin science from molecules to population health · 2024Article
- Origin and Function of Monocytes in Inflammatory Bowel Disease.Journal of inflammation research · 2024Review
- Humanized NSG Mouse Models as a Preclinical Tool for Translational Research in Inflammatory Bowel Diseases.International journal of molecular sciences · 2023Article
- CD1a promotes systemic manifestations of skin inflammation.Nature communications · 2022Article
- NOD/scid IL-2RγImmunity, inflammation and disease · 2021Article
- Suppressing Kv1.3 Ion Channel Activity with a Novel Small Molecule Inhibitor Ameliorates Inflammation in a Humanised Mouse Model of Ulcerative Colitis.Journal of Crohn's & colitis · 2021Article
- Identification of SARS-CoV-2-specific immune alterations in acutely ill patients.The Journal of clinical investigation · 2021Article
- Role of Group 1 CD1-Restricted T Cells in Host Defense and Inflammatory Diseases.Critical reviews in immunology · 2021Article
- Does CD1a Expression Influence T Cell Function in Patients With Langerhans Cell Histiocytosis?Frontiers in immunology · 2021Article
- Protective effect of Gloeostereum incarnatum on ulcerative colitis via modulation of Nrf2/NF‑κB signaling in C57BL/6 mice.Molecular medicine reports · 2020Article
- The Combination of Patient Profiling and Preclinical Studies in a Mouse Model Based on NOD/Scid IL2Rγ null Mice Reconstituted With Peripheral Blood Mononuclear Cells From Patients With Ulcerative Colitis May Lead to Stratification of Patients for Treatment With Adalimumab.Inflammatory bowel diseases · 2020Article
- Autoantibodies as diagnostic markers and potential drivers of inflammation in ulcerative colitis.PloS one · 2020Article
- Article
- Targeting ulcerative colitis by suppressing glucose uptake with ritonavir.Disease models & mechanisms · 2018Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCD1a-expressing CD14+ monocytes have been identified as inducers of autoreactive T cells. In this study, the link between inflammatory and metabolic signals and CD1a-expressing monocytes in vitro and in vivo was examined, and CD1a was evaluated as a potential therapeutic target for treatment of ulcerative colitis (UC).
methodsPeripheral blood mononuclear cells (PBMCs) from UC patients and non-UC donors were incubated with phosphatidylcholine (PC) for 2 and 7 days and subjected to flow cytometric analysis. Triacylglycerol (TAG) and cholesterol levels and frequencies of CD14+ CD1a+ monocytes were determined in a mouse model of UC that is based on NOD/scid IL2Rγnull mice reconstituted with PBMCs from UC patients (NSG-UC). NSG-UC mice were treated with anti-CD1a antibodies. Response to treatment was determined by clinical and histological scores, flow cytometric analysis of human leucocytes from the spleen and colon, and expression levels of TGFß1, HGF, IFNγ, and TARC.
resultsIncubation of PBMCs with PC resulted in an increase of the frequency of CD1a+ CD14+ monocytes at the expense of CCR2-, CD86-, and TSLPR-expressing CD14+ monocytes. CD1a+ CD14+ monocytes induced the activation of CD4+ T cells and differentiation of Th cells. In vivo, TAG and cholesterol levels increased upon inflammation and correlated positively with CD14+ CD1a+ monocytes. NSG-UC mice benefitted from treatment with anti-CD1a antibodies, as indicated by a reduced histological score and reduced frequencies of CD1a+ CD14+ monocytes in the colon and spleen of mice.
conclusionCD1a-expressing monocytes might act as sensors and mediators of inflammation in UC. Mice benefitted from treatment with anti-CD1a antibodies.
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