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. 1982 May;45(5):737–746. doi: 10.1038/bjc.1982.115

Mononuclear-cell infiltration in ovarian cancer. II. Immune function of tumour and ascites-derived inflammatory cells.

S Haskill, H Koren, S Becker, W Fowler, L Walton
PMCID: PMC2011003  PMID: 6177328

Abstract

Mononuclear cell fractions were isolated from blood, ascites and solid tumours of patients undergoing surgery for Stages III and IV adenocarcinoma of the ovary, and evaluated for their response in NK, ADCC and PHA assays. Control experiments with the same fraction of normal blood indicated that these responses were not influenced by the enzymes used to isolate the tumour and ascites inflammatory cells. The inflammatory cell fractions isolated from both tumour sites which sedimented in the velocity range of blood mononuclear cells were adequate in number and composition for comparison with similar cells from blood. E RFC values in both ascites and tumour fractions exceeded those of patient blood. However, there was a marked difference in distribution of the T subsets between blood, ascites and tumour, which could cause the variable test results between the different cell sources. PHA responses of patient blood and ascites fractions were about half that of normal blood. Tumour-infiltrating lymphocytes (TIL) were less than 10% as responsive as normal blood. The depressed PHA responses of the TIL were not due to the presence of a suppressor cell population. NK activity of patient blood was less than that of normal blood, but not as much as the ascites of TIL cells. The activity of the ascites-derived lymphocytes was enhanced by treatment with interferon. ADCC activity against both CRBC and SB cells was normal or higher than controls in patient blood, and depressed in the ascites-derived fractions. TIL responded to less than 10% of the patient blood values. The results indicate a lack of response by ascitic and TIL cells in assays dependent on FcR-bearing effector cells and a greater loss of PHA-reactive cells from the tumour than from blood and ascites. These data could result from intratumour inactivation, or a failure of the particular subset to localize either in the ascites or the tumour site.

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Selected References

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