Different T Cell Receptor Signals Determine CD8 + Memory Versus Effector Development

Author:

Teixeiro Emma12345,Daniels Mark A.12345,Hamilton Sara E.12345,Schrum Adam G.12345,Bragado Rafael12345,Jameson Stephen C.12345,Palmer Ed12345

Affiliation:

1. Experimental Transplantation Immunology, Department of Biomedicine, University Hospital-Basel, Hebelstrasse 20, 4031-Basel, Switzerland.

2. Department of Molecular Microbiology and Immunology, University of Missouri, School of Medicine, Center for Cellular and Molecular Immunology, Columbia, MO 65212, USA.

3. Center for Immunology and Department of Laboratory Medicine and Pathology, University of Minnesota Medical School, Minneapolis, MN 55454, USA.

4. Department of Immunology, Fundación Jiménez Díaz, Avenida Reyes Católicos 2, 28040-Madrid, Spain.

5. Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905,USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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