A transcription factor PU.1 is critical for Ccl22 gene expression in dendritic cells and macrophages
Open accessAbstract
The chemokine CCL22 is predominantly produced by dendritic cells (DCs) and macrophages. CCL22 acts on CCR4-expressing cells including Th2 and Treg. Although a correlation between the CCL22-CCR4 axis and allergic diseases has been established, the mechanism of monocyte lineage-specific Ccl22 gene expression is largely unknown. In the current study, we investigated transcriptional regulation of the Ccl22 gene in DCs and macrophages. Using reporter assays, we identified the critical cis-enhancing elements at 21/−18 and −10/−4 in the Ccl22 promoter. Electrophoretic mobility shift assays proved that transcription factor PU.1 directly binds to the cis-elements. Knockdown of PU.1 markedly decreased Ccl22 expression in bone marrow-derived DCs (BMDCs) and BM macrophages (BMDMs). Chromatin immunoprecipitation assays revealed that PU.1 bound to the Ccl22 promoter in not only BMDCs and BMDMs, but also splenic DCs and peritoneal macrophages. LPS stimulation increased the amount of PU.1 recruited to the promoter, accompanied by upregulation of the Ccl22 mRNA level, which was diminished by Spi1 knockdown. We identified similar cis-elements on the human CCL22 promoter, which were bound with PU.1 in human monocytes. Taken together, these findings indicate that PU.1 transactivates the Ccl22 gene in DCs and macrophages by directly binding to the two elements in the promoter.
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PU.1 confers an inflammatory phenotype to B cells and macrophages.
“By initiating the expression of pro-inflammatory cytokines, PU.1 confers an inflammatory phenotype to B cells and macrophages [12,13,14].”
From Ectopic PU.1 Expression Provides Chimeric Antigen Receptor (CAR) T Cells with Innate Cell Capacities Including IFN-β Release (2024) · cites this paper as [14]
The Discussion (page not provided) shows that PU.1 regulates Ccl22 expression in macrophages, but identifies Ccl22 as an M2 macrophage marker rather than evidence that PU.1 confers an inflammatory phenotype. The Introduction (page not provided) mentions PU.1 in B-cell development and TNF-α regulation in dendritic cells; it does not establish pro-inflammatory cytokine expression or an inflammatory phenotype in B cells and macrophages. (LLM, conf=0.86)
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- Authors
- Yashiro, T., Nakano, S., Nomura, K., Uchida, Y., Kasakura, K., & Nishiyama, C.
- Affiliations
- Tokyo University of Science (JP)
- Corresponding author
- Nishiyama, Chiharu
- Venue
- Scientific Reports
- Published
- 2019-02-04
- Volume
- 9
- Issue
- 1
- Pages
- 1161-1161
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6361964
- OpenAlex
- W2937351235
- Cited by
- 29
- References
- 38
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 6 · 2023: 1 · 2022: 4 · 2021: 3 · 2020: 6 · 2019: 2
- FWCI
- 2.40
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Takeda Science Foundation
- Tokyo Biochemical Research Foundation
- Ministry of Education, Culture, Sports, Science and Technology
- Tojuro Iijima Foundation for Food Science and Technology
- Japan Society for the Promotion of Science (16J03241, 17K15276)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- PU.1, CCL22, chemokine expression, dendritic cells, macrophages, transcriptional regulation, promoter cis-acting elements, CCR4, allergic diseases, monocytes, lipopolysaccharide stimulation, transcription factor binding
- MeSH terms
- RAW 264.7 Cells, THP-1 Cells, Proto-Oncogene Protein Spi-1, Animals, Dendritic Cells, Humans, Macrophages, Mice, Inbred BALB C, Promoter Regions, Genetic, Proto-Oncogene Proteins, Trans-Activators, Up-Regulation, Mice, Chemokine CCL22
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