Journal
JOURNAL OF IMMUNOLOGY
Volume 191, Issue 12, Pages 5797-5801Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1300905
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Funding
- University of Missouri Life Sciences fellowship
- Leukemia and Lymphoma Society Career Development Program
- University of Missouri Mission Enhancement Fund
- University of Missouri Research Board
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CD8 T cell memory critically contributes to long-term immunity. Both low- and high-affinity TCR signals are able to support the differentiation of memory CD8 T cells. However, it is unclear whether the requirements for memory development change when TCR signal strength is altered. To gain further insight into this question, we used a TCR beta transmembrane domain mutant model that is defective in the generation of memory in response to high-affinity ligands. Surprisingly, lowering TCR signal strength, by stimulation with low- affinity ligands, resulted in normal memory development. Restoration of memory correlated with recovery of TCR-dependent NF-kappa B signaling. Thus, these data provide novel evidence that the requirements for memory are qualitatively different depending on TCR signal strength.
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