Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1
Abstract
Adaptive immunity depends on T-cell exit from the thymus and T and B cells travelling between secondary lymphoid organs to survey for antigens. After activation in lymphoid organs, T cells must again return to circulation to reach sites of infection; however, the mechanisms regulating lymphoid organ exit are unknown. An immunosuppressant drug, FTY720, inhibits lymphocyte emigration from lymphoid organs, and phosphorylated FTY720 binds and activates four of the five known sphingosine-1-phosphate (S1P) receptors. However, the role of S1P receptors in normal immune cell trafficking is unclear. Here we show that in mice whose haematopoietic cells lack a single S1P receptor (S1P1; also known as Edg1) there are no T cells in the periphery because mature T cells are unable to exit the thymus. Although B cells are present in peripheral lymphoid organs, they are severely deficient in blood and lymph. Adoptive cell transfer experiments establish an intrinsic requirement for S1P1 in T and B cells for lymphoid organ egress. Furthermore, S1P1-dependent chemotactic responsiveness is strongly upregulated in T-cell development before exit from the thymus, whereas S1P1 is downregulated during peripheral lymphocyte activation, and this is associated with retention in lymphoid organs. We find that FTY720 treatment downregulates S1P1, creating a temporary pharmacological S1P1-null state in lymphocytes, providing an explanation for the mechanism of FTY720-induced lymphocyte sequestration. These findings establish that S1P1 is essential for lymphocyte recirculation and that it regulates egress from both thymus and peripheral lymphoid organs.
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CD69 inhibits the function of S1PR1, which is required for S1P-mediated egress into the blood.
“CD69 inhibits the function of S1PR1, which is required for S1P-mediated egress into the blood [260-262].”
From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [261]
S1P is the primary chemoattractant that drives the exit of activated and recirculating lymphocytes from lymph nodes into efferent LVs.
“S1P is the primary chemoattractant that drives the exit of activated and recirculating lymphocytes from lymph nodes into efferent LVs (106, 122, 123).”
From Transport and Immune Functions of the Lymphatic System. (2025) · cites this paper as [122]
FTY720-P modulates S1P receptors (S1PRs) to reduce their cell surface expression and signaling.
“In contrast to S1P, FTY720-P modulates S1P receptors (S1PRs) to reduce their cell surface expression and signaling (50).”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [50]
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- Authors
- Matloubian, M., Lo, C. G., Cinamon, G., Lesneski, M. J., Xu, Y., Brinkmann, V., Allende, M. L., Proia, R. L., & Cyster, J. G.
- Affiliations
- Howard Hughes Medical Institute (US)
- Novartis (Switzerland) (CH)
- National Institutes of Health (US)
- Corresponding author
- Cyster, Jason G.
- Venue
- Nature
- Published
- 2004-01
- Volume
- 427
- Issue
- 6972
- Pages
- 355-360
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2006985918
- Cited by
- 2,581
- References
- 24
- Citations by year
- 2026: 64 · 2025: 75 · 2024: 82 · 2023: 94 · 2022: 109 · 2021: 130 · 2020: 119 · 2019: 130 · 2018: 101 · 2017: 122 · 2016: 138 · 2015: 124 · 2014: 177 · 2013: 127 · 2012: 143
- FWCI
- 41.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Keywords
- S1P1 receptor, sphingosine-1-phosphate, lymphocyte egress, thymus, secondary lymphoid organs, T cell emigration, lymphocyte migration, lymphocyte recirculation, fingolimod, chemotaxis, lymphocyte sequestration, T cell development
- MeSH terms
- Fingolimod Hydrochloride, Animals, Cell Movement, Chemotaxis, Chimera, Lymphocyte Activation, Lymphocytes, Lymphoid Tissue, Lysophospholipids, Propylene Glycols, Sphingosine, Thymus Gland, Down-Regulation, Gene Deletion, Mice, Knockout, Adoptive Transfer, Receptors, G-Protein-Coupled, Receptors, Lysophospholipid, Mice
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