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Open Access Publications from the University of California

Scholarly Works (3 results)

  • Article
  • Peer Reviewed
UC San Francisco Previously Published Works (2018)
An antibody overcomes cancer cell immune evasion and activates natural killer cells
    Cover page: Natural killers join the fight against cancer
    • Article
    • Peer Reviewed
    UC San Francisco Previously Published Works (2016)
    Immunological memory can be defined as a quantitatively and qualitatively enhanced immune response upon rechallenge. For natural killer (NK) cells, two main types of memory exist. First, similarly to T cells and B cells, NK cells can exert immunological memory after encounters with stimuli such as haptens or viruses, resulting in the generation of antigen-specific memory NK cells. Second, NK cells can remember inflammatory cytokine milieus that imprint long-lasting non-antigen-specific NK cell effector function. The basic concepts derived from studying NK cell memory provide new insights about innate immunity and could lead to novel strategies to improve treatments for infectious diseases and cancer.
      Cover page: Natural killer cell memory in infection, inflammation and cancer
      • Article
      • Peer Reviewed
      UC San Francisco Previously Published Works (2005)

      The expression of the Adenovirus serotype 5 ( Ad5) E1A oncogene sensitizes tumor cells to natural killer ( NK) cell - mediated killing and tumor rejection in vivo. These effects are dependent on the ability of E1A to bind the transcriptional coadaptor protein p300. To test the hypothesis that E1A up- regulates ligands recognized by the NKG2D- activating receptor, we stably transfected the highly tumorigenic mouse fibrosarcoma cell line MCA- 205 with Ad5- E1A or a mutant form of E1A that does not interact with p300 ( E1A- Delta p300). Ad5- E1A, but not E1A- Delta p300, up- regulated the expression of the NKG2D ligand retinoic acid early inducible ( RAE)- 1, but not murine ULBP- like transcript 1, another NKG2D ligand, in four independently derived MCA- 205 transfectants. The up- regulation of RAE- 1 by E1A targeted MCA- 205 tumor cells to lysis by NK cells, resulting in NKG2D- dependent tumor rejection in vivo. Moreover, the up- regulation of NKG2D ligands by E1A was not limited to mouse tumor cells, as E1A also increased the expression of NKG2D ligands on primary baby mouse kidney cells, human MB435S breast cancer cells, and human H4 fibrosarcoma cells.

        Cover page: Adenovirus serotype 5 E1A sensitizes tumor cells to NKG2D-dependent NK cell lysis and tumor rejection
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