L
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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Role of ITAM-containing adapter proteins and their receptors in the immune system and bone.
TL;DR: Regulation of osteoclastogenesis by ITAM‐dependent receptors suggests that OCLs, similar to related myeloid cells, are tightly controlled by arrays of receptors that allow them to sense and respond to their local microenvironment like other innate immune cells.
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The developmental relationship between NK cells and T cells.
TL;DR: Recent studies of fetal ontogeny and thymic development that provide support for the hypothesis that NK cells and T cells have a common origin are described and an integrated scheme for NK-cell and T-cell development is proposed.
Journal Article
Molecular and functional analysis of human natural killer cell-associated neural cell adhesion molecule (N-CAM/CD56).
Lewis L. Lanier,Chiwen Chang,Miyuki Azuma,Joyce J. Ruitenberg,J. J. Hemperly,Joseph H. Phillips +5 more
TL;DR: It was determined that expression of N-CAM on these target cells does not affect susceptibility to resting or IL-2-activated NK cell-mediated cytotoxicity and heterotypic lymphocyte-tumor cell adhesion, and homophilic N-cAM interactions probably do not mediate a major role in the cytolytic interaction between NK cells and N- CAM+ tumor cell targets.
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Paraformaldehyde fixation of hematopoietic cells for quantitative flow cytometry (FACS) analysis.
Lewis L. Lanier,Noel L. Warner +1 more
TL;DR: This method was suitable for all cell types analyzed, including mouse, human and rat lymphoid cells, erythrocytes and transformed cell lines, and could prove useful to those who work with in vivo derived specimens or have limited access to flow cytometry facilities.
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Phosphotyrosines in the killer cell inhibitory receptor motif of NKB1 are required for negative signaling and for association with protein tyrosine phosphatase 1C.
TL;DR: It is demonstrated that KIR can not only inhibit cytolytic activity, but can also negatively regulate T cell receptor activation events that lead to downstream gene activation, and further supports a model that implicates PTP1C as a mediator in the KIR inhibitory signal.