Mucosal immunology, 2019-09, Vol.12 (5), p.1104-1117
2019
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- Autor(en) / Beteiligte
- Titel
- JunB plays a crucial role in development of regulatory T cells by promoting IL-2 signaling
- Ist Teil von
- Mucosal immunology, 2019-09, Vol.12 (5), p.1104-1117
- Ort / Verlag
- New York: Nature Publishing Group US
- Erscheinungsjahr
- 2019
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- The AP-1 transcription factor JunB plays crucial roles in multiple biological processes, including placental formation and bone homeostasis. We recently reported that JunB is essential for development of Th17 cells, and thus Junb -deficient mice are resistant to experimental autoimmune encephalomyelitis. However, the role of JunB in CD4 + T cells under other inflammatory disease conditions is unknown. Here we show that mice lacking JunB in CD4 + T cells ( Junb fl/fl Cd4-Cre mice) were more susceptible to dextran sulfate sodium (DSS)-induced colitis because of impaired development of regulatory T (Treg) cells. Production of interleukin (IL)-2 and expression of CD25, a high affinity IL-2 receptor component, were decreased in Junb -deficient CD4 + T cells in vitro and in vivo. Naive CD4 + T cells from Junb fl/fl Cd4-Cre mice failed to differentiate into Treg cells in the absence of exogenously added IL-2 in vitro. A mixed bone marrow transfer experiment revealed that defective Treg development of Junb -deficient CD4 + T cells was not rescued by co-transferred wild-type cells, indicating a significance of the cell-intrinsic defect. Injection of IL-2-anti-IL-2 antibody complexes induced expansion of Treg cells and alleviated DSS-induced colitis in Junb fl/fl Cd4-Cre mice. Thus JunB plays a crucial role in the development of Treg cells by facilitating IL-2 signaling.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1933-0219eISSN: 1935-3456DOI: 10.1038/s41385-019-0182-0Titel-ID: cdi_proquest_journals_2282779500
- Format
- –
- Schlagworte
- Activator protein 1, Allergology, Animals, Antibodies, Binding Sites, Biomedical and Life Sciences, Biomedicine, Bone growth, Bone marrow, Bone turnover, CD25 antigen, CD4 antigen, Cell differentiation, Colitis, Colitis - etiology, Colitis - metabolism, Colitis - pathology, Dextran, Dextran sulfate, Dextran Sulfate - adverse effects, Disease Models, Animal, Experimental allergic encephalomyelitis, Gastroenterology, Gene Expression Profiling, Gene Expression Regulation, Helper cells, Homeostasis, Immunology, Immunoregulation, Inflammatory bowel disease, Inflammatory diseases, Interferon-gamma - metabolism, Interleukin 2, Interleukin 2 receptors, Interleukin-2 - metabolism, JunB protein, Lymphocytes, Lymphocytes T, Mice, Mice, Transgenic, Placenta, Protein Binding, Signal Transduction, T-Lymphocyte Subsets - immunology, T-Lymphocyte Subsets - metabolism, T-Lymphocytes, Regulatory - immunology, T-Lymphocytes, Regulatory - metabolism, Transcription factors, Transcription Factors - metabolism