Abstract
Following infection, naïve CD8+ T cells bearing pathogen-specific T cell receptors (TCRs) differentiate into a mixed population of short-lived effector and long-lived memory T cells to mediate an adaptive immune response. How the TCR regulates memory T cell development has remained elusive. Using a mutant TCR transgenic model, we found that point mutations in the TCR β transmembrane domain (βTMD) impair the development and function of CD8+ memory T cells without affecting primary effector T cell responses. Mutant T cells are deficient in polarizing the TCR and in organizing the nuclear factor κB signal at the immunological synapse. Thus, effector and memory states of CD8+ T cells are separable fates, determined by differential TCR signaling.
Original language | English (US) |
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Pages (from-to) | 502-505 |
Number of pages | 4 |
Journal | Science |
Volume | 323 |
Issue number | 5913 |
DOIs | |
State | Published - Jan 23 2009 |
ASJC Scopus subject areas
- General