Abstract
A hallmark of mammalian immunity is the heterogeneity of cell fate that exists among pathogen-experienced lymphocytes. We show that a dividing T lymphocyte initially responding to a microbe exhibits unequal partitioning of proteins that mediate signaling, cell fate specification, and asymmetric cell division. Asymmetric segregation of determinants appears to be coordinated by prolonged interaction between the T cell and its antigen-presenting cell before division. Additionally, the first two daughter T cells displayed phenotypic and functional indicators of being differentially fated toward effector and memory lineages. These results suggest a mechanism by which a single lymphocyte can apportion diverse cell fates necessary for adaptive immunity.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adoptive Transfer
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Animals
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Antigen Presentation
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Antigens, CD / analysis
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CD8 Antigens / analysis
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CD8-Positive T-Lymphocytes / cytology*
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CD8-Positive T-Lymphocytes / immunology*
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Cell Differentiation
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Cell Division*
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Cell Lineage
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Cell Polarity
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Dendritic Cells / immunology
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Immunologic Memory*
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Interferon gamma Receptor
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Intracellular Signaling Peptides and Proteins / metabolism
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Listeria monocytogenes / immunology
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Listeriosis / immunology
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Lymphocyte Activation
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Membrane Proteins / analysis
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Mitosis
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Nerve Tissue Proteins / analysis
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Protein Kinase C / metabolism
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Receptors, Antigen, T-Cell / immunology
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Receptors, Interferon / analysis
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Signal Transduction
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T-Lymphocyte Subsets / cytology*
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T-Lymphocyte Subsets / immunology*
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T-Lymphocytes, Helper-Inducer / immunology
Substances
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Antigens, CD
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CD8 Antigens
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Intracellular Signaling Peptides and Proteins
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Membrane Proteins
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Nerve Tissue Proteins
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Numb protein, mouse
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Receptors, Antigen, T-Cell
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Receptors, Interferon
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scribble protein, mouse
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protein kinase C zeta
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Protein Kinase C