AbstractIntraperitoneal injection of Group A streptococcal cell wall (SCW) fragments into female Lewis rats results in the induction of an acute hepatic inflammation that progresses to granulomatous lesions. Kupffer cells have been shown to rapidly clear circulating SCW which triggers production of TGF-β. In this study, we examined Kupffer cells for the expression of TGF-βreceptors to determine if these cells might be modulated in an autocrine/paracrine fashion by TGF-βduring SCW-hepatic inflammation. By receptor crosslinking and subsequent SDS-PAGE analysis we demonstrate that Kupffer cells express Type I TGF-βreceptors, but not Types II and III. Scatchard analysis indicated a receptor density of approximately 1100 receptors per cell. Functionally, TGF-βwas found to be chemotactic for Kupffer cellsin vitroand this chemotactic response was higher in cells isolated from rats 1–21 days post SCW-injection. Although TGF-β1 mRNA is constitutively expressed by Kupffer cells,in vitrostimulation of the cultures with purified TGF-βaugments the expression of TGF-β1 mRNA and protein synthesis suggesting autocrine/paracrine regulation. These results indicate that TGFβsecreted by Kupffer cells during SCW-induced hepatic inflammation may amplify its own expression and regulate Kupffer cell functions relevant to the formation of granulomatous lesions within the liver.