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Lewis L. Lanier

Researcher at University of California, San Francisco

Publications -  576
Citations -  93495

Lewis L. Lanier is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Interleukin 21 & Natural killer cell. The author has an hindex of 159, co-authored 554 publications receiving 86677 citations. Previous affiliations of Lewis L. Lanier include University of Rome Tor Vergata & Cancer Research Institute.

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Proinflammatory cytokine signaling required for the generation of natural killer cell memory

TL;DR: Responsiveness to interleukin-12, but not interferon-γ, is essential for the generation of long-lived natural killer cells capable of responding to secondary viral infection.
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Cross-Talk between Activated Human NK Cells and CD4+ T Cells via OX40-OX40 Ligand Interactions

TL;DR: This study shows that OX40 ligand is selectively induced on IL-2, IL-12, or IL-15-activated human NK cells following stimulation through NKG2D, the low affinity receptor for IgG (CD16) or killer cell Ig-like receptor 2DS2, providing direct evidence for cross-talk between human CD4+ T cells and NK receptor-activated NK cells.
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Ligands for natural killer cell receptors: redundancy or specificity.

TL;DR: A better understanding about how targets signal their distress, which renders them susceptible to natural killer (NK)‐cell attack, will help to define the role of NK cells in antimicrobial and antitumor immunity and transplantation.
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Arousal and inhibition of human NK cells

TL;DR: The membrane receptors on human NK cells that are known to initiate cell‐mediated cytotoxicity are reviewed and regulation of these responses by the killer cell inhibitory (KIR) receptors is demonstrated.
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Molecular definition of the identity and activation of natural killer cells

TL;DR: Using whole-genome microarray data sets of the Immunological Genome Project, the authors demonstrate a closer transcriptional relationship between NK cells and T cells than between any other leukocytes, distinguished by their shared expression of genes encoding molecules with similar signaling functions.