Effector CD4 T-cell transition to memory requires late cognate interactions that induce autocrine IL-2

K. Kai McKinstry (), Tara M. Strutt, Bianca Bautista, Wenliang Zhang, Yi Kuang, Andrea M. Cooper and Susan L. Swain
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K. Kai McKinstry: University of Massachusetts Medical School
Tara M. Strutt: University of Massachusetts Medical School
Bianca Bautista: University of Massachusetts Medical School
Wenliang Zhang: University of Massachusetts Medical School
Yi Kuang: University of Massachusetts Medical School
Andrea M. Cooper: Trudeau Institute
Susan L. Swain: University of Massachusetts Medical School

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract It is unclear how CD4 T-cell memory formation is regulated following pathogen challenge, and when critical mechanisms act to determine effector T-cell fate. Here, we report that following influenza infection most effectors require signals from major histocompatibility complex class II molecules and CD70 during a late window well after initial priming to become memory. During this timeframe, effector cells must produce IL-2 or be exposed to high levels of paracrine or exogenously added IL-2 to survive an otherwise rapid default contraction phase. Late IL-2 promotes survival through acute downregulation of apoptotic pathways in effector T cells and by permanently upregulating their IL-7 receptor expression, enabling IL-7 to sustain them as memory T cells. This new paradigm defines a late checkpoint during the effector phase at which cognate interactions direct CD4 T-cell memory generation.

Date: 2014
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DOI: 10.1038/ncomms6377

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