TIM4 (T cell immunoglobulin mucin domain molecule-4) plays a critical role in the initiation of skewed T helper (Th) 2 polarization. The factors regulating TIM4 expression are unclear. This study tests a hypothesis that p300 and STAT6 (signal transducer and activator transcription-6) regulates TIM4 expression in dendritic cells (DC). In this study, a food allergy mouse model was developed with ovalbumin (a specific antigen) and cholera toxin (CT; an adjuvant). The chromatin immunoprecipitation assay was performed to evaluate the chromatin changes at TIM4 and STAT6 promoters. The TIM4 expression was evaluated by real time RT-PCR and Western blotting. The results showed that high levels of p300 and TIM4 were detected in the intestinal DCs of mice with intestinal allergy. p300 is involved in the CT-induced TIM4 expression in DCs. p300 interacts with the chromatin at the TIM4 promoter locus in DCs isolated from allergic mice. CT increases p300 expression to regulate STAT6 levels in DCs. STAT6 mediates the CT-induced TIM4 expression in DCs. In conclusion, p300 and STAT6 mediate the microbial product CT-induced TIM4 expression in DCs.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761958 | PMC |
| http://dx.doi.org/10.1038/srep21336 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dust mite antigens endow dendritic cells with the capacity to induce a Th2 response by regulating their methylation profiles.
Cell Commun Signal
December 2024
Department of Otolaryngology of Longgang Central Hospital and Clinical College Affiliated to Guangzhou University of Chinese Medicine, Shenzhen, China.
Background: It is well-known that Dendritic cells (DCs) are essential in the development of airway Th2 polarization and airway allergy (AA). The underlying mechanism is still not fully understood. The objective of this study is to examine the role of methyltransferase-like protein-5 (Mettl5), a methyltransferase involved in N6-methyladenosine (m6A) methylation, in altering DC's properties to facilitate the development of Th2 polarization and AA.
View Article and Find Full Text PDFRetention of ES cell-derived 129S genome drives NLRP1 hypersensitivity and transcriptional deregulation in Nlrp3 mice.
Cell Death Differ
December 2024
Institute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Article Synopsis
- Immune response genes vary widely among humans and mice, leading to different defense responses based on genetic differences, which can complicate research outcomes.
- This study used RNA sequencing and variant analysis to uncover significant genetic variations in a commonly used mouse model of NLRP3 deficiency, highlighting the impact of the Nlrp1 locus on macrophage activation independently of the NLRP3 status.
- The research provides a method to identify important genetic variations and evaluate contamination in transgenic mice studies, enhancing the reliability of findings in host defense research.
Angelica sinensis polysaccharides ameliorate 5-FU-induced stress anemia via promoting extramedullary erythroblastic island central macrophage-mediated erythroid differentiation.
Int Immunopharmacol
December 2024
Laboratory of Stem Cells and Tissue Engineering, Department of Histology and Embryology, Chongqing Medical University, Chongqing 400016, China. Electronic address:
Article Synopsis
- Chronic anemia, especially from chemotherapy, is a serious problem that can be hard to treat and can cause side effects from traditional treatment options.
- Researchers studied how a substance from a Chinese herb called Angelica sinensis (ASP) helps mice recover from anemia caused by the chemotherapy drug 5-fluorouracil (5-FU).
- The study found that ASP helped mice produce more red blood cells and other blood components by improving their bone marrow and spleen function, showing that it could be a helpful treatment for anemia caused by cancer treatments.
TIM-4 increases the proportion of CD4CD25FOXP3 regulatory T cells in the pancreatic ductal adenocarcinoma microenvironment by inhibiting IL-6 secretion.
Cancer Med
September 2024
Division of Pancreatic Surgery, Department of General Surgery, West China Hospital, Sichuan University, Chengdu, China.
Background: Currently, creating more effector T cells and augmenting their functions is a focal point in pancreatic ductal adenocarcinoma (PDAC) treatment research. T cell immunoglobulin domain and mucin domain molecule 4 (TIM-4), known for promoting cancer progression in various malignancies, is implicated in the suppressive immune microenvironment of tumors. Analyzing of the role of TIM-4 in the immune regulation of PDAC can offer novel insights for immune therapy.
View Article and Find Full Text PDFUnlabelled: Fidelity of wound healing after myocardial infarction (MI) is an important determinant of subsequent adverse cardiac remodeling and failure. Macrophages derived from infiltrating Ly6C blood monocytes are a key component of this healing response; however, the importance of other macrophage populations is unclear. Here, using a variety of in vivo murine models and orthogonal approaches, including surgical myocardial infarction, splenectomy, parabiosis, cell adoptive transfer, lineage tracing and cell tracking, RNA sequencing, and functional characterization, we establish in mice an essential role for splenic CD169 Tim4 marginal metallophilic macrophages (MMMs) in post-MI wound healing.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!