Publications by authors named "Wiebke Rackwitz"

NK cells are endowed with tumor killing ability, nevertheless most cancers impair NK cell functionality, and cell-based therapies have limited efficacy in solid tumors. How cancers render NK cell dysfunctional is unclear, and overcoming resistance is an important immune-therapeutic aim. Here, we identify autophagy as a central regulator of NK cell anti-tumor function.

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Article Synopsis
  • NK cells can be made more effective against tumors through targeting with antibodies or genetic modifications, but some tumors still resist attacks, particularly in the context of the ErbB2 (HER2) antibody trastuzumab.
  • In experiments, using NK-92 cells and primary human NK cells, functions like cell killing and cytokine release were diminished when LFA-1 was blocked or ICAM-1 was absent during ADCC triggered by trastuzumab, but CAR-engineered NK cells showed resilience against these disruptions.
  • The study found that while trastuzumab needed LFA-1 to fully activate NK cells, the ErbB2-CAR provided a strong activation on its own, leading to effective tumor targeting, and
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Natural killer (NK) cells are attractive effectors for adoptive immunotherapy of cancer. Results from first-in-human studies using chimeric antigen receptor (CAR)-engineered primary NK cells and NK-92 cells are encouraging in terms of efficacy and safety. In order to further improve treatment strategies and to test the efficacy of CAR-NK cells in a personalized manner, preclinical screening assays using patient-derived tumor samples are needed.

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Background: Colistin is still a widely used antibiotic in veterinary medicine although it is a last-line treatment option for hospitalized patients with infections caused by multidrug-resistant Gram-negative bacteria. Colistin resistance has gained additional importance since the recent emergence of mobile colistin resistance () genes. In the scope of a study on colistin resistance in clinical isolates from human patients in Germany we characterized the - gene variants.

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