TGF-β1 Reciprocally Controls Chemotaxis of Human Peripheral Blood Monocyte-Derived Dendritic Cells Via Chemokine Receptors
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We examined the effect of TGF-β1 on the chemotactic migratory ability of human monocyte-derived dendritic cells (DCs). Treatment of immature DCs with TGF-β1 resulted in increased expressions of CCR-1, CCR-3, CCR-5, CCR-6, and CXC chemokine receptor-4 (CXCR-4), which were concomitant with enhanced chemotactic migratory responses to their ligands, RANTES (for CCR-1, CCR-3, and CCR-5), macrophage-inflammatory protein-3α (MIP-3α) (for CCR-6), or stromal cell-derived growth factor-1α (for CXCR-4). Ligation by TNF-α resulted in down-modulation of cell surface expressions of CCR-1, CCR-3, CCR-5, CCR-6, and CXCR-4, and the chemotaxis for RANTES, MIP-3α, and stromal cell-derived growth factor-1α, whereas this stimulation up-regulated the expression of CCR-7 and the chemotactic ability for MIP-3β. Stimulation of mature DCs with TGF-β1 also enhanced TNF-α-induced down-regulation of the expressions of CCR-1, CCR-3, CCR-5, CCR-6, and CXCR-4, and chemotaxis to their respective ligands, while this stimulation suppressed TNF-α-induced expression of CCR-7 and chemotactic migratory ability to MIP-3β. Our findings suggest that TGF-β1 reversibly regulates chemotaxis of DCs via regulation of chemokine receptor expression.
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Dendritic cells in the intestine can promote regulatory T cell development via TGF-β activation, perhaps through integrin αvβ8.
“Additionally, intestinal DCs can induce Treg cell differentiation through activation of TGF-β, possibly involving cell-intrinsic expression of integrin αvβ8186,187.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [187]
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- Authors
- Sato, K., Kawasaki, H., Nagayama, H., Enomoto, M., Morimoto, C., Tadokoro, K., Juji, T., & Takahashi, T. A.
- Affiliations
- Institute of Medical Science, The University of Tokyo (JP)
- Japanese Red Cross Society, Japan (JP)
- Corresponding author
- Sato, Katsuaki
- Nagayama, Hitomi
- Enomoto, Makoto
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-03-01
- Volume
- 164
- Issue
- 5
- Pages
- 2285-2295
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1483423516
- Cited by
- 152
- References
- 53
- Citations by year
- 2024: 2 · 2023: 3 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 9
- FWCI
- 5.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- TGF-β1, dendritic cells, monocyte-derived dendritic cells, chemotaxis, chemokine receptors, CCR5, CXCR4, RANTES, TNF-α, dendritic cell maturation, receptor down-regulation
- MeSH terms
- Cell Differentiation, Cell Membrane, Cells, Cultured, Chemotaxis, Leukocyte, Dendritic Cells, Humans, Ligands, Monocytes, Tumor Necrosis Factor-alpha, Down-Regulation, Up-Regulation, Immunophenotyping, Transforming Growth Factor beta, Interleukin-10, Macrophage Inflammatory Proteins, Receptors, Chemokine, Receptors, CCR5, Receptors, CXCR4, Chemokines, CC, Receptors, CCR1, Receptors, CCR3, Receptors, CCR6, Receptors, CCR7, Chemokine CCL19, Chemokine CCL20, CCR5 Receptor Antagonists
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