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Both K\u2010562 and Sk\u2010v cells were killed by a non\u2010adherent CD16<jats:sup>+<\/jats:sup> subset of PBMC as revealed by cell fractionation on the basis of their adherence to plastic and by treatment with Leu\u2010IIb monoclonal antibody (MAb) and complement. \u201cCold\u201d target competitive assays demonstrated that both cell types inhibited lysis of labelled Sk\u2010v cells. In patients with BP and anogenital carcinomas induced by HPV\u201016 or 33, there was a significant (at least at <jats:italic>p<\/jats:italic> &lt; 0.01) decrease of Sk\u2010v cell lysis as compared with the healthy control group. Anti\u2010K\u2010562 activity was not affected. In patients with anogenital carcinomas the degree of Sk\u2010v lysis was decreased in proportion to the duration of lesions (correlation coefficient\u2013r = \u20100.79). Neither anti\u2010K\u2010562 nor anti\u2010Sk\u2010v cytotoxicities were significantly affected in patients with condylomata and with HPV\u20106 associated verrucous carcinomas. Short\u2010term (3 hr) pre\u2010incubation of normal PBMC with sera from patients with BP and HPV\u201016\u2010associated anogenital carcinomas resulted in significant inhibition of their ability to lyse Sk\u2010v cells. Lysis of K\u2010562 cells remained unaffected. In patients with carcinomas, the suppressive effect of sera was associated with a lowering of the ability of their PBMC to lyse Sk\u2010v cells (r = \u20100.79). In patients with longer tumor persistence, the suppressive effect of serum was proportionally higher (r = 0.86).<\/jats:p>","DOI":"10.1002\/ijc.2910430206","type":"journal-article","created":{"date-parts":[[2007,2,19]],"date-time":"2007-02-19T21:10:22Z","timestamp":1171919422000},"page":"209-214","source":"Crossref","is-referenced-by-count":39,"title":["Abrogated NK\u2010cell lysis of human papillomavirus (HPV)\u201016\u2010bearing keratinocytes in patients with pre\u2010cancerous and cancerous HPV\u2010induced anogenital lesions"],"prefix":"10.1002","volume":"43","author":[{"given":"Jacek","family":"Malejczyk","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Slawomir","family":"Majewski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefania","family":"Jablonska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomasz T.","family":"Rogozinski","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerard","family":"Orth","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,17]]},"reference":[{"key":"e_1_2_1_2_1","first-page":"85","article-title":"The modulation of human natural killer cell activity by prostaglandins","volume":"7","author":"Bankhurst A. 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