Monoclonal antibodies (mAb) were prepared against conjugated transforming growth factor β1 (TGFβ1) peptides: amino acid positions 48–60 and positions 86–101. Two antibodies, mAb 16-3G1 [anti-(48–60)] and mAb 5-2G6 [anti-(86–101)] cross-reacted with native TGFβ1,-β2 and-β3 (16-3G1) or only with native TGFβ1 (5-2G6). Both mAb were used to characterize TGFβ-mediated effects on the metastatic potential in nude mice of human carcinoma cell line SLU-1 and its metastatic subline SLU-M1. Autocrine TGFβ1-mediated up-regulation of cell proliferation and its suppression by anti-TGFβ antibodies in vitro was recorded for SLU-M1 cells whereas SLU-1 cell proliferation in vitro appeared to be refractory to anti-TGFβ antibodies and exogenous TGF-β1. However, the potential of s.c. tumours to develop distant metastases in nude mice was about the same for both cell lines. Development of primary tumours and distant metastases could be suppressed by treatment of mice with anti-TGFβ antibodies. Thus we assume that the metastatic potential of tumour cells is independent of TGFβ-mediated growth-regulation effects in vitro. The anti-TGFβ-induced suppression of tumour progression and metastasis in nude mice might rather result from stimulation of the immune surveillance. TGFβ-mediated autocrine down-regulation of MHC-unrestricted cytotoxicity of activated human monocytes and CD56⁺ LAK cells and its reversion by anti-TGFβ antibodies could be readily demonstrated. In all our experimental series, the neutralizing potential of both anti-TGFβ antibodies, though directed against opposite sites of the TGFβ1 molecule, was very similar.