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Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the production of antinuclear autoantibodies. Antinuclear autoantibody development is recognized as one of the initial stages of disease that often results in systemic inflammation, kidney disease, and death. The etiology is complex, but it is clear that innate pathways may play an important role in disease progression. Recent data have highlighted an important role for the TLR family, particularly TLR7, in both human disease and murine models. In this study, we have presented a low copy conditional TLR7 transgenic (Tg7) mouse strain that does not develop spontaneous autoimmunity. When we combine Tg7 with the Sle1 lupus susceptibility locus, the mice develop severe disease. Using the CD19(Cre) recombinase system, we normalized expression of TLR7 solely within the B cells. Using this method we demonstrated that overexpression of TLR7 within the B cell compartment reduces the marginal zone B cell compartment and increases B and T cell activation but not T follicular helper cell development. Moreover, this enhanced B cell TLR7 expression permits the specific development of Abs to RNA/protein complexes and exacerbates SLE disease.

Original publication





Journal of immunology (Baltimore, Md. : 1950)

Publication Date





5786 - 5796


Department of Immunology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA.


B-Lymphocyte Subsets, Animals, Mice, Inbred C57BL, Mice, Transgenic, Humans, Mice, Lupus Erythematosus, Systemic, Disease Progression, Genetic Predisposition to Disease, Multiprotein Complexes, Membrane Glycoproteins, Autoantibodies, Epistasis, Genetic, Gene Expression Regulation, Developmental, Transgenes, Female, Male, Toll-Like Receptor 7, Mice, 129 Strain