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Transforming growth factor-beta1 (TGF-beta1) is released during the storage of blood components, particularly platelet concentrates, and transfusion recipients are exposed to high levels of TGF-beta1. Because TGF-beta1 is one of the most potent immunosuppressive cytokines known, understanding the immunobiologic functions of TGF-beta1 may be relevant for understanding the immunobiologic effects of transfusion. Our laboratory studies the biologic effects of TGF-beta1 in the immune system. Mice deficient in TGF-beta1 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-beta1-/- mice. TGF-beta1-/- mice on the BALB/c background rapidly develop an aggressive T-cell-mediated hepatitis, whereas TGF-beta1-/- 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in press from our laboratory on disease pathogenesis in TGF-beta1-/- mice and then discuss some of the exciting (as-yet-unpublished) directions our laboratory is currently taking.
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James D. Gorham (2005) studied this question.
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