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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Evidence for NK Cell Subsets Based on Chemokine Receptor Expression
TL;DR: Within both the CD56bright and CD56dim NK cell populations, subsets with the capacity for differential trafficking programs exist, which likely influence their functions in innate and adaptive immunity.
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Differential Expression of Leukocyte Receptor Complex-Encoded Ig-Like Receptors Correlates with the Transition from Effector to Memory CTL
TL;DR: Results indicate a sequential program of LRC-encoded receptor expression with initial ILT2/LIR1 expression in effector T cells and KIR gene transcription in the minor proportion of expanded clones which survives activation-induced cell death to become long term memory T cells.
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Nonfunctional mutants of the retinoblastoma protein are characterized by defects in phosphorylation, viral oncoprotein association, and nuclear tethering
TL;DR: It is concluded that mutations in two distinct regions of the protein concomitantly affect four aspects of p110Rb function, including binding to the E1A oncoprotein, hyperphosphorylated, tightly associated with nuclear structures, and ability to induce senescent cells in Saos-2 human osteosarcoma cells.
Journal Article
Involvement of CD28 in MHC-unrestricted cytotoxicity mediated by a human natural killer leukemia cell line.
TL;DR: The concept that MHC-unrestricted cytotoxicity may not be due to a unique receptor, but may result from interactions between an appropriate array of "adhesion" molecules with their ligands is supported.
Journal Article
Conserved and variable residues within the Bw4 motif of HLA-B make separable contributions to recognition by the NKB1 killer cell-inhibitory receptor.
Jenny E. Gumperz,L. D. Barber,Nicholas Valiante,L Percival,Joseph H. Phillips,Lewis L. Lanier,Peter Parham +6 more
TL;DR: Mutation at leucine 82 and arginine 83, the residues common to Bw4 motifs, shows they contribute to N KB1 interaction but are not essential, and three types of polymorphism are implicated in formation of the ligand recognized by NKB1.