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Cited by 145T-cell and B-cell ImmunologyCell Adhesion Molecules ResearchImmune Cell Function and Interaction

A potential role for CD69 in thymocyte emigration

Feng, Chiguang, Woodside, Kenneth J., Vance, Barbara A., El‐Khoury, Dalal, Canelles, Matilde, Lee, Jan, Gress, Ronald, Fowlkes, B. J. +2 more·2002·International Immunology
DOI 10.1093/intimm/dxf020
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Abstract

The early activation marker, CD69, is transiently expressed on activated mature T cells and on thymocytes that are undergoing positive or negative selection in the thymus. CD69 is a member of the NK gene complex family of C-type lectin-like signaling receptors; however, its function is unknown. In this report, we describe the characterization of mice that constitutively express high levels of surface CD69 on immature and mature T cells throughout development. Constitutive surface expression of CD69 did not affect T cell maturation, signaling through the TCR or thymocyte selection. However, phenotypically and functionally mature thymocytes accumulated in the medulla of CD69 transgenic mice and failed to be exported from the thymus. The retention of mature thymocytes correlated with transgene dose and CD69 surface levels. These results identify a potential role for CD69 in controlling thymocyte export, and suggest that the transient expression of CD69 on thymocytes and T cells may function to regulate thymocyte and T cell trafficking.

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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 [262]

    The Abstract (page unavailable) reports that mature thymocytes accumulated in CD69-transgenic mice and failed to leave the thymus. The Discussion (page unavailable) proposes that CD69 may inhibit their export, but does not identify S1PR1 or an S1P-mediated mechanism. Searches for S1PR1 and sphingosine-1-phosphate found no passage supporting that specific mechanism. (LLM, conf=0.88)

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Authors
Feng, C., Woodside, K. J., Vance, B. A., El‐Khoury, D., Canelles, M., Lee, J., Gress, R., Fowlkes, B. J., Shores, E. W., & Love, P. E.
Affiliations
  • National Institutes of Health (US)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (US)
  • National Cancer Institute (MY)
Corresponding author
Feng, Chiguang
ORCID
Venue
International Immunology
Publisher
Oxford University Press (OUP)
Published
2002-06
Volume
14
Issue
6
Pages
535-544
ISSN
  • 0953-8178 (ISSN-L)
  • 1460-2377
DOI
10.1093/intimm/dxf020
OpenAlex
W2155048915
Cited by
145
References
39
Citations by year
2026: 2 · 2025: 3 · 2024: 2 · 2023: 8 · 2022: 6 · 2021: 7 · 2020: 5 · 2019: 5 · 2018: 3 · 2017: 5 · 2016: 2 · 2015: 6 · 2014: 3 · 2013: 4 · 2012: 10
FWCI
2.84
Type
journal article
Language
en
Open access
closed
Locations
  • International Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
Keywords
CD69, thymocyte emigration, thymic medulla, T cell migration, thymic selection, T cell development, C-type lectin-like receptors, transgenic mice, T cell activation markers
MeSH terms
CD69 Antigens, Animals, Antigens, Differentiation, T-Lymphocyte, Cell Differentiation, Cell Movement, Cell Survival, Humans, Kinetics, Mice, Inbred C57BL, Mice, Transgenic, Phenotype, T-Lymphocytes, Thymus Gland, Antigens, CD, T-Lymphocyte Subsets, Mice, Knockout, Lectins, C-Type, Mice

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