{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:55:10Z","timestamp":1791093310999,"version":"4.1.0"},"reference-count":72,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2002,5,13]],"date-time":"2002-05-13T00:00:00Z","timestamp":1021248000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2002,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>MICA, a highly glycosylated membrane\u2010anchored cell\u2013surface MHC Class I\u2010related chain, has recently been reported to activate NK cell cytolytic responses in epithelial tumors. Tumor cells may escape from NK lysis by counteracting NK cytotoxicity activating signals with inhibitory ones. Among the molecules that mediate an NK inhibitory signal, HLA\u2010G1, a non\u2010classical MHC Class I antigen, is of particular interest. HLA\u2010G1 is ectopically expressed in various tumors, including melanoma and constitutes the major NK inhibitory ligand in the M8 melanoma cell line when coexpressed with HLA\u2010A, \u2010B, \u2010C and \u2010E molecules. We have evaluated the balance between 2 powerful signals that affect NK cell tumor lysis, one inhibitory and the other one activating, respectively HLA\u2010G1 and MICA. For this purpose, we transfected the M8 melanoma cell line, which spontaneously expresses MICA, with HLA\u2010G1 cDNA, using it as a target for the NKL effector. We carried out cytotoxicity assays, using antibodies that disrupt interactions between the MICA and HLA\u2010G1 ligands and their respective NK effector counterparts, the NKG2D activating and ILT2 inhibitory receptors. Results showed that 1) MICA expressed in the M8 melanoma cell line triggered NK cell tumor lysis and 2) HLA\u2010G1 coexpression mediated the inhibition of NK cytotoxicity by mitigating the MICA activating signal. HLA\u2010G1 expression in a tumor cell line in which MICA is switched on would therefore appear to be a powerful way to turn off NK cells, supporting the emerging idea that the balance between positive and negative NK cytolysis signals critically influences tumor progression. \u00a9 2002 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.10460","type":"journal-article","created":{"date-parts":[[2002,10,6]],"date-time":"2002-10-06T12:27:22Z","timestamp":1033907242000},"page":"63-70","source":"Crossref","is-referenced-by-count":86,"title":["MICA triggering signal for NK cell tumor lysis is counteracted by HLA\u2010G1\u2010mediated inhibitory signal"],"prefix":"10.1002","volume":"100","author":[{"given":"Catherine","family":"Menier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u00e9atrice","family":"Riteau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edgardo 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