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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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Cutting Edge: Inhibition of TLR and FcR Responses in Macrophages by Triggering Receptor Expressed on Myeloid Cells (TREM)-2 and DAP12

TL;DR: It is shown that Triggering Receptor Expressed on Myeloid cells (TREM)-2 is responsible for the DAP12-mediated inhibition in mouse macrophages and the interaction of TREM-2 and its ligand results in an inhibitory signal that can reduce the inflammatory response.
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Co-association of CD3ζ with a receptor (CD16) for IgG Fc on human natural killer cells

TL;DR: It is reported that CD16, the receptor for the Fc (constant) region of IgG, specifically associates with the CD3ζ homodimer on the membrane of human NK cells, and that co-transfection with CD 3ζ complementary DNA permits expression of a transmembrane-linked CD 16 complex on COS-7 cells.
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LAIR-1, a Novel Inhibitory Receptor Expressed on Human Mononuclear Leukocytes

TL;DR: Although it is structurally related to human killer cell inhibitory receptors, LAIR-1 does not appear to recognize human leukocyte antigen (HLA) class I molecules and thus represents a novel HLA class I-independent mechanism of NK cell regulation.
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Injured sensory neuron-derived CSF1 induces microglial proliferation and DAP12-dependent pain

TL;DR: It is found that peripheral nerve injury induced de novo expression of colony-stimulating factor 1 (CSF1) in injured sensory neurons and the microglial membrane adaptor protein DAP12 was required for both nerve injury– and intrathecal CSF1–induced upregulation of pain-related microglia genes and the ensuing pain, but not formicroglial proliferation.
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B7 and interleukin 12 cooperate for proliferation and interferon gamma production by mouse T helper clones that are unresponsive to B7 costimulation.

TL;DR: It is shown that IL-12 can overcome the inhibitory effect of IL-10 for the APC-dependent induction of proliferation and IFN-gamma production by Th1 clones and may help to maintain these T cells in an unresponsive state during an inflammatory response.