Authors:
Emma Teixeiro, Mark A. Daniels, Sara E. Hamilton, Adam G. Schrum, Rafael Bragado, Stephen C. Jameson, & Ed Palmer
Summary:
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 B signal at the immunological synapse. Thus, effector and memory states of CD8+ T cells are separable fates, determined by differential TCR signaling.
Source:
Science; Vol. 323, No. 5913 502-505 (01/23/09)