Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 215, Issue 5, Pages 1481-1492Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20171708
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Funding
- Technology Core of the Center for Translational Science at Institut Pasteur
- Institut Pasteur
- Institut National de la Sante et de la Recherche Medicale
- European Research Council
- Ligue Contre le Cancer
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T cells are primed in secondary lymphoid organs by establishing stable interactions with antigen-presenting cells (APCs). However, the cellular mechanisms underlying the termination of T cell priming and the initiation of clonal expansion remain largely unknown. Using intravital imaging, we observed that T cells typically divide without being associated to APCs. Supporting these findings, we demonstrate that recently activated T cells have an intrinsic defect in establishing stable contacts with APCs, a feature that was reflected by a blunted capacity to stop upon T cell receptor (TCR) engagement. T cell unresponsiveness was caused, in part, by a general block in extracellular calcium entry. Forcing TCR signals in activated T cells antagonized cell division, suggesting that T cell hyporesponsiveness acts as a safeguard mechanism against signals detrimental to mitosis. We propose that transient unresponsiveness represents an essential phase of T cell priming that promotes T cell disengagement from APCs and favors effective clonal expansion.
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