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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Journal ArticleDOI
CEACAM1 on activated NK cells inhibits NKG2D‐mediated cytolytic function and signaling
Shuhei Hosomi,Zhangguo Chen,Zhangguo Chen,Kristi Baker,Lanfen Chen,Yu-Hwa Huang,Torsten Olszak,Sebastian Zeissig,Jing Wang,Ofer Mandelboim,Nicole Beauchemin,Lewis L. Lanier,Richard S. Blumberg +12 more
TL;DR: Carcinoembryonic antigen‐related cell adhesion molecule 1 on activated NK cells functions as an inhibitory receptor for NKG2D‐mediated cytolysis, which has important implications for understanding the means by which CEACAM1 expression adversely affects tumor immunity.
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A human natural killer cell-associated antigen defined by monoclonal antibody anti-Leu (NKP-15): functional and two-color flow cytometry analysis.
TL;DR: The existence of a cell surface antigen common to granulocytes and NK cells, which is capable of distinguishing subpopulations of Leu 7 + cells, provides a useful probe to analyze the nature of the NK lineage.
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EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production
April Kalinowski,Iris F. Ueki,Gundula Min-Oo,Eric Ballon-Landa,David S. Knoff,Benjamin T. Galen,Lewis L. Lanier,Jay A. Nadel,Jonathan L. Koff +8 more
TL;DR: It is reported that respiratory virus-induced EGFR activation suppresses CXCL10 production, a novel mechanism that viruses use to suppress endogenous antiviral defenses, and provide potential targets for future therapies.
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CALGB 150905 (Alliance): Rituximab Broadens the Antilymphoma Response by Activating Unlicensed NK Cells
Juan Du,Sandra López-Vergès,Brandelyn N. Pitcher,Jeffrey L. Johnson,Sin-Ho Jung,Lili Zhou,Katharine C. Hsu,Myron S. Czuczman,Bruce D. Cheson,Lawrence D. Kaplan,Lewis L. Lanier,Jeffrey M. Venstrom +11 more
TL;DR: The clinical efficacy of rituximab may be driven, in part, by its ability to broaden the NK-cell repertoire to include previously hyporesponsive, unlicensed NK cells, and a “missing ligand” KIR and HLA class I genotype may be predictive of this benefit and useful for personalizing treatment decisions in lymphomas and other tumors.
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Intact NKG2D-independent function of NK cells chronically stimulated with the NKG2D ligand Rae-1.
Marine Champsaur,Joshua N. Beilke,Kouetsu Ogasawara,Ulrich H. Koszinowski,Stipan Jonjić,Lewis L. Lanier +5 more
TL;DR: It is shown that constant exposure to NKG2D ligands does not functionally impair NK cells and CD8+ T cells in the context of viral infection.