TCF1 expression marks self-renewing human CD8 + T cells.
| Autor: | Kratchmarov R; Department of Microbiology and Immunology and.; Department of Pediatrics, Roy and Diana Vagelos College of Physicians and Surgeons, Columbia University, New York, NY., Magun AM; Division of Digestive and Liver Diseases, Department of Medicine, Columbia University Medical Center, New York, NY., Reiner SL; Department of Microbiology and Immunology and.; Department of Pediatrics, Roy and Diana Vagelos College of Physicians and Surgeons, Columbia University, New York, NY. |
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| Jazyk: | angličtina |
| Zdroj: | Blood advances [Blood Adv] 2018 Jul 24; Vol. 2 (14), pp. 1685-1690. |
| DOI: | 10.1182/bloodadvances.2018016279 |
| Abstrakt: | Expression of the transcription factor T-cell factor 1 (TCF1) identifies antigen-experienced murine CD8 + T cells that retain potential for lymphoid recirculation and the ability to self-renew while producing more differentiated effector cells. We found that CD8 + T cells in the blood of both healthy and chronically infected humans expressed TCF1 at 3 distinct levels: high (TCF1-hi), intermediate (TCF1-int), and low (TCF1-lo). TCF1-hi cells could be found within both the naive and memory compartments and were characterized by relative quiescence and lack of immediate effector function. A substantial fraction of TCF1-int cells were found among memory cells, and TCF1-int cells exhibited robust immediate effector functions. TCF1-lo cells were most enriched in effector memory cells that expressed the senescence marker CD57. Following reactivation, TCF1-hi cells gave rise to TCF1-lo descendants while self-renewing the TCF1-hi progenitor. By contrast, reactivation of TCF1-lo cells produced more TCF1-lo cells without evidence of de-differentiating into TCF1-hi cells. Flow cytometric analyses of TCF1 expression from patient specimens may become a useful biomarker for adaptive immune function in response to vaccination, infection, autoimmunity, and cancer. (© 2018 by The American Society of Hematology.) |
| Databáze: | MEDLINE |
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