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外文期刊>european journal of immunology
>Cytological and functional analysis of inflammatory infiltrates in human malignant tumors II. Functional investigations of the infiltrating inflammatory cells
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Cytological and functional analysis of inflammatory infiltrates in human malignant tumors II. Functional investigations of the infiltrating inflammatory cells
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机译:Cytological and functional analysis of inflammatory infiltrates in human malignant tumors II. Functional investigations of the infiltrating inflammatory cells
AbstractSix individual human carcinomas displaying an unusually strong inflammatory reaction were dispersed by a mixture of collagenase and deoxyribonuclease and fractionated in 1 × g velocity sedimentation. This method gave an excellent separation of cancer cells from infiltrating inflammatory cells. The viability in both cell populations exceeded 95%. Blood mononuclear leukocytes and tumor‐infiltrating inflammatory cells from the cancer‐bearing patients were then tested in the short‐term51Cr release test forin vitrocytotoxicity to their autochtonous tumor cells and to target cells known to be sensitive to the socalled “natural killer” (NK) lytic effects. In two patients with testicular seminoma, the blood leukocytes were strongly cytotoxic to the patients' own tumor cells; in one case of thyroid carcinoma, the patient's blood leukocytes also exhibited a distinct albeit slight cytotoxic activity towards his autochtonous tumor. Blood mononuclear leukocytes of all these cancer patients were strongly cytotoxic to the NK targets MOLT‐4, K‐562, chicken red cells and human embryonic fibroblasts (Ef). In striking contrast, the tumor‐infiltrating inflammatory cells were entirely unable to lyse the autologous tumor cells. Neither, with the exception of the Ef targets, did the tumor‐infiltrating cells display any cytotoxic activity towards the NK targets. The findings demonstrate a widespread functional paralysis (or absence) of effector cells directed to the patients' own autologous tumor cells and to NK target cells in the tumor‐infiltrating inflamma
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