This is a double transgenic system in which expression of a pseudo-autoantigen is controlled by a tet responsive element (TRE) and expression of the corresponding transactivator is controlled by a tissue specific promoter.
eBook Title: A Tet-regulatable Mouse Model for the Analysis of Systemic Autoimmune Disease
Author:Karen Sunhae Lee
Published on 2008 by
Abstract: The major challenge of systemic autoimmune diseases like systemic lupus erythematosus (SLE) or systemic sclerosis (SSc), has been understanding the transition from early events of elaboration of autoantibody, to tissue fibrosis and end-organ damage. In order to determine whether the microenvironment regulates the pathologic consequences of an autoimmune response, we generated a novel mouse model that allows for the manipulation of the site and level of expression of a pseudo-autoantigen. This is a double transgenic system in which expression of a pseudo-autoantigen is controlled by a tet responsive element (TRE) and expression of the corresponding transactivator is controlled by a tissue specific promoter. Further, the timing and level of expression can be controlled by the administration of doxycycline (dox). Our pseudo-autoantigen is a fusion protein that incorporates the transferrin receptor, GFP and ovalbumin (TGO) recognized by DO11.10 CD4 + T cells. We have developed divergent mouse models of autoimmune disease by directing the expression of the pseudo-autoantigen to distinct tissue locales. In one model, expression of TGO is directed to MHC class II-positive cells. Here, the intravenous transfer of DO11.10 TH2 cells initiates an SLE-like disease, characterized by the production of anti-nuclear autoantibodies (ANA) that deposit in the kidney and cause immune complex-mediated glomerulonephritis. Intriguingly, we can limit the development of disease by removing dox from the drinking water, implicating the importance of T cell recognition of the pseudo-autoantigen in sustained autoantibody production. In the second model TGO expression is directed to the vascular endothelium. Here, the transfer of TH1 or TH17 DO11.10 T cells can trigger a disease phenotype characterized by pathogenic changes in the skin and lung. For example, TH1 DO11.10 T cells induce lung fibrosis, while TH17 cells trigger pulmonary vasculopathy, both features of SSc. Having demonstrated that these mouse models can mimic distinct systemic autoimmune disease phenotypes, they will enable us to more effectively delineate the specific conditions that promote SLE or SSc pathology.
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Karen Sunhae Lee
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