Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 206, Issue 2, Pages 275-285Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20080996
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Funding
- Lucille P. Markey Stanford Graduate Fellowship
- Siegelman Fellowship for Pediatric Research
- Pediatric Children's Health Research Award
- Department of Pediatrics, Stanford University
- Jeffrey Model Foundation for Primary Immunodeficiency
- National Institutes of Health [R21 HD37589]
- Howard Hughes Medical Institute
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CD4+ recent thymic emigrants (RTEs) comprise a clinically and immunologically important T cell population that indicates thymic output and that is essential for maintaining a diverse alpha beta-T cell receptor (TCR) repertoire of the naive CD4(+) T cell compartment. However, their frequency and function are poorly understood because no known surface markers distinguish them from older non-RTE naive CD4(+) T cells. We demonstrate that protein tyrosine kinase 7 (PTK7) is a novel marker for human CD4(+) RTEs. Consistent with their recent thymic origin, human PTK7(+) RTEs contained higher levels of signal joint TCR gene excision circles and were more responsive to interleukin (IL)-7 compared with PTK7(-) naive CD4(+) T cells, and rapidly decreased after complete thymectomy. Importantly, CD4+ RTEs proliferated less and produced less IL-2 and interferon-gamma than PTK7(-) naive CD4(+) T cells after alpha gamma TCR/CD3 and CD28 engagement. This immaturity in CD4(+) RTE effector function may contribute to the reduced CD4(+) T cell immunity observed in contexts in which CD4(+) RTEs predominate, such as in the fetus and neonate or after immune reconstitution. The ability to identify viable CD4(+) RTEs by PTK7 staining should be useful for monitoring thymic output in both healthy individuals and in patients with genetic or acquired CD4(+) T cell immunodeficiencies.
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