Tumour-derived soluble MIC ligands impair expression of NKG2D and T-cell activation

By V. Groh, Jennifer D. Wu, C. Yee, T. Spies. Nature, 2002

1,646 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/1e9cab8e60d433da279aabefedc158228ca2c8e7

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Citations in the corpus

Lactate in the Regulation of Tumor Microenvironment and Therapeutic Approaches (2019, background): “Nevertheless, tumor cells inhibit the activation of NK cells triggered by lacking of MCH class I expression through the release of soluble molecules such as MHC class I chainrelated protein A (MICA) and MHC class I chain-related protein B (MICB), which bind to the activator receptor (NKG2D) on NK ce”
Immune functions encoded by the natural killer gene complex (2003, background): “The induced expression of NKG2D ligands on tumours seems to be counterproductive from the tumour viewpoin”
Regulation of ligands for the NKG2D activating receptor (2013, background): “Initially, soluble MICA was detected in the sera of patients with lung, breast, and gastrointestinal malignancies (107, 108), and cell-free forms of MICA and MICB were subsequently detected in patients with a variety of cancers (109–115).”
Exosome-Based Cell-Cell Communication in the Tumor Microenvironment (2018, background): “Accordingly, Groh et al. showed that cancer patients exhibit a decrease of NKG2D surface expression on circulating NK cells in comparison with healthy individuals (Groh et al., 2002).”
Adoptive transfer of effector CD8+ T cells derived from central memory cells establishes persistent T cell memory in primates. (2008, background): “The isolation of tumor-reactive T cells from cancer patients is difficult due to their low frequency and/or functional impairments in the tumor-bearing host (43, 44).”