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Summary Using an under agarose migration (UAM) assay, we studied lymphokine-activated killer (LAK)-attractant activity in cultured conditioned medium of tumour tissues after chemotherapy as a possible mechanism of enhanced LAK cell accumulation into tumour tissues after chemotherapy. BMT-11 is a fibrosarcoma developed in C57BL/6 mice. The conditioned medium of BMT-11 tumour tissues obtained from mice treated with various anti-cancer drugs had chemotactic activity for LAK cells (LAK-attractant activity). mRNA expression of interleukin (IL)-la, IL-6, IL-8, interferon (IFN)-y, and tumour necrosis factor (TNF)-a was observed in untreated tumour tissues, which were not enhanced by cyclophosphamide treatment. mRNA expression of TGF-,IB was not detected in untreated tumour tissues by reverse transcription-polymerase chain reaction (RT-PCR), but was detected in tumour tissues treated with cyclophosphamide. Recombinant human TGF-,B1 showed LAK-attractant activity at a concentration of 0.1 ng ml-1 and 1 ng ml-', whereas fresh splenocytes were not attracted by TGF-f,1. Anti-TGF-,B1 antibody inhibited LAK-attractant activity in the conditioned medium of tumour tissues treated with cyclophosphamide to approximately 35% that of control at 100 Mg ml -l. These findings indicate that TGF-,13 produced in the tumour tissues of mice treated with anticancer drugs could be a LAK attractant. By a 4 h 51 Cr release assay of natural killer cell-resistant BMT-11 tumour cells, we observed that TGF-,B1 at a concentration from 0.01 ng ml-1 to 10 ng ml-1 did not inhibit LAK activity in an effector phase. Taken together, we suggest that TGF-,B1 produced in tumour tissues after chemotherapy participates in gathering transferred LAK cells and contributes to the therapeutic effects of transferred LAK cells.

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