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CD8+ T cells play a crucial role in controlling intracellular pathogens. The level of memory CD8+ T cells developing after vaccination or infection influences the degree of T cell-mediated protection after secondary infection. We used defined animal models and infections/immunizations by replicating or non-replicating antigens to define on a molecular and cellular level in vivo the parameters that identify and shape long-lived CD8+ T cell memory. We show that the timing of antigen exposure during vaccination is key for the induction of long-lived T cell memory. Brief antigen exposure induced high numbers of effector cells but limited development of long-lived CD8+ memory T cells. In contrast, prolonged antigen exposure for up to 9 days induced similar numbers of effector T cells but additionally resulted in high levels of memory CD8+ T cells. Unexpectedly CD127 (IL-7Ralpha) expression on CD8+ T cells during the acute priming phase was a necessary but not sufficient requirement for entering the pool of long-lived antigen-independent memory CD8+ T cells. However, we provide strong evidence for the interpretation that programming of long-lived memory T cells was driven by low levels of transcription factor eomesodermin and protease inhibitor Spi2A as well as reduced phosphorylation of c-JUN.

Original publication




Journal article


Eur J Immunol

Publication Date





842 - 854


Animals, Antigens, Antigens, Viral, CD8-Positive T-Lymphocytes, Fluorescent Antibody Technique, Gene Expression, Immunologic Memory, JNK Mitogen-Activated Protein Kinases, Lymphocyte Activation, Lymphocytic choriomeningitis virus, Mice, Mice, Inbred C57BL, Phosphorylation, Receptors, Interleukin-7, Reverse Transcriptase Polymerase Chain Reaction, Serpins, T-Box Domain Proteins, Vaccines, Xenopus Proteins