Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 8, Pages 4921-4930Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0901226
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Funding
- Swedish Foundation for Strategic Research
- Swedish Society for Medical Research
- Swedish Research Council
- Swedish Cancer Society
- Swedish Children's Cancer Foundation
- Cancer Society of Stockholm
- Ake Wiberg Foundation
- Royal Swedish Academy of Science
- Tobias Foundation
- Mary Beve Foundation
- David and Astrid Hagelens Foundation
- Abney Foundation
- Stockholm City Council
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The activating NK cell receptor DNAX accessory molecule-1 (DNAM-1) contributes to tumor immune surveillance and plays a crucial role in NK cell-mediated recognition of several types of human tumors, including ovarian carcinoma. Here, we have analyzed the receptor repertoire and functional integrity of NK cells in peritoneal effusions from patients with ovarian carcinoma. Relative to autologous peripheral blood NK cells, tumor-associated INK cells expressed reduced levels of the DNAM-1, 2134, and CD16 receptors and were hyporesponsive to HILA class I-deficient K562 cells and to coactivation via DNAM-1 and 2B4. Moreover, tumor-associated NK cells were also refractory to CD16 receptor stimulation, resulting in diminished Ab-dependent cellular cytotoxicity against autologous tumor cells. Coincubation of INK cells with ovarian carcinoma cells expressing the DNAM-1 ligand CD155 led to reduction of DNAM-1 expression. Therefore, NK cell-mediated rejection of ovarian carcinoma may be limited by perturbed DNAM-l expression on tumor-associated NK cells induced by chronic ligand exposure. Thus, these data support the notion that tumor-induced alterations of activating INK cell receptor expression may hamper immune surveillance and promote tumor progression. The Journal of Immunology, 2009, 183: 4921-4930.
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