Transforming growth factor‐β1, Th1 responses, and autoimmune liver disease

Transforming growth factor‐β1 (TGF‐β1) is released during the storage of blood components, particularly platelet concentrates, and transfusion recipients are exposed to high levels of TGF‐β1. Because TGF‐β1 is one of the most potent immunosuppressive cytokines known, understanding the immunobiologic functions of TGF‐β1 may be relevant for understanding the immunobiologic effects of transfusion. Our laboratory studies the biologic effects of TGF‐β1 in the immune system. Mice deficient in TGF‐β1 spontaneously develop autoimmunity, confirming the important role of this cytokinean an immune regulator. A few years ago, my laboratory made the observation that genetic background strongly affects the phenotype of TGF‐β1–/– mice. TGF‐β1–/– mice on the BALB/c background rapidly develop an aggressive T‐cell–mediated hepatitis, whereas TGF‐β1–/– mice on the 129/CF‐1 background do not. In this review, I summarize findings published or in press from our laboratory on disease pathogenesis in TGF‐β1–/– mice and then discuss some of the exciting (as‐yet‐unpublished) directions our laboratory is currently taking.