An experimental therapy for improvement of macrophage dysfunction caused by transforming growth factor‐β (TGF‐β) was tried in EL4 tumor‐bearing mice. TGF‐β was detected in cell‐free ascitic fluid from EL4‐bearers, but not in tbat from normal mice, by western blot analysis. The ascites also showed growth‐suppressive activity against MvlLn cells, and the suppressive activity was potentiated by transient acidification. To investigate whether the functions of peritoneal macrophagcs were suppressed in EL4‐bearers, the abilities to produce nitric oxide and tumor necrosis factor‐α (TNF‐α) upon lipopolysaccharide (LPS) stimulation were measured. Both abilities of macrophages in EL4‐bearing mice were suppressed remarkably on day 9, and decreased further by day 14, compared with non‐tumor‐bearing controls. TGF‐β activity was abrogated by administration of anti‐TGF‐α antibody to EL4‐bearing mice. While a large amount of TGF‐β was detected in ascitic fluid from control EL4‐bearers, little TGF‐β was detectable in ascites from EL4‐bearers given anti‐TGF‐β antibody. Furthermore, while control macrophages exhibited little or no production of nitric oxide and TNF‐α on LPS stimulation in vitro, macrophages from EL4‐bearers administered with anti‐TGF‐β antibody showed the same ability as normal macrophages. These results clearly indicate that TGF‐β contributes to macrophage dysfunction and that the administration of specific antibody for TGF‐β reverses macrophage dysfunction in EL4‐bearing hosts.