Abstract
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 TCRβ 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-κB signaling. Thus, these data provide novel evidence that the requirements for memory are qualitatively different depending on TCR signal strength.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Active Transport, Cell Nucleus
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Adoptive Transfer
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Animals
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Antigens / immunology
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CD8-Positive T-Lymphocytes / immunology*
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CD8-Positive T-Lymphocytes / transplantation
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Gene Expression Regulation / immunology
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Immunologic Memory / immunology*
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Immunomagnetic Separation
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Ligands
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Listeria monocytogenes / immunology
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Listeriosis / immunology
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Lymphocyte Count
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Lymphopenia / immunology
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Lymphopoiesis
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Mice
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Mice, Congenic
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Mice, Inbred C57BL
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Mice, Transgenic
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NF-kappa B / physiology
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Ovalbumin / immunology
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Peptide Fragments / immunology
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Point Mutation
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Protein Structure, Tertiary / genetics
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Receptors, Antigen, T-Cell, alpha-beta / chemistry
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Receptors, Antigen, T-Cell, alpha-beta / genetics
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Receptors, Antigen, T-Cell, alpha-beta / immunology*
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T-Lymphocyte Subsets / immunology*
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T-Lymphocyte Subsets / transplantation
Substances
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Antigens
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Ligands
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NF-kappa B
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Peptide Fragments
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Receptors, Antigen, T-Cell, alpha-beta
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Ovalbumin