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Cited by 152Chemokine receptors and signalingTGF-β signaling in diseasesImmunotherapy and Immune Responses

The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.

TGF-β1 Reciprocally Controls Chemotaxis of Human Peripheral Blood Monocyte-Derived Dendritic Cells Via Chemokine Receptors

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Sato, Katsuaki, Kawasaki, Hiroshi, Nagayama, Hitomi, Enomoto, Makoto, Morimoto, Chikao, Tadokoro, Kenji, Juji, Takeo, Takahashi, Tsuneo A·2000·The Journal of Immunology
DOI 10.4049/jimmunol.164.5.2285
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Abstract

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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Metadata

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
ORCID
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
DOI
10.4049/jimmunol.164.5.2285
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
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
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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