Toll-like Receptor 7 and TLR9 Dictate Autoantibody Specificity and Have Opposing Inflammatory and Regulatory Roles in a Murine Model of Lupus
Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis i...
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| Published in | Immunity (Cambridge, Mass.) Vol. 25; no. 3; pp. 417 - 428 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.09.2006
Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis in susceptible mice. We report that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag. TLR9 and TLR7 also had dramatic effects on clinical disease in lupus-prone mice. In the absence of TLR9, autoimmune disease was exacerbated, lymphocytes and plasmacytoid DCs were more activated, and serum IgG and IFN-α were increased. In contrast, TLR7-deficient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG. These findings reveal opposing inflammatory and regulatory roles for TLR7 and TLR9, despite similar tissue expression and signaling pathways. These results have important implications for TLR-directed therapy of autoimmune disease. |
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| AbstractList | Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis in susceptible mice. We report that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag. TLR9 and TLR7 also had dramatic effects on clinical disease in lupus- prone mice. In the absence of TLR9, autoimmune disease was exacerbated, lymphocytes and plasmacytoid DCs were more activated, and serum IgG and IFN- alpha were increased. In contrast, TLR7-deficient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG. These findings reveal opposing inflammatory and regulatory roles for TLR7 and TLR9, despite similar tissue expression and signaling pathways. These results have important implications for TLR-directed therapy of autoimmune disease. Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis in susceptible mice. We report that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag. TLR9 and TLR7 also had dramatic effects on clinical disease in lupus-prone mice. In the absence of TLR9, autoimmune disease was exacerbated, lymphocytes and plasmacytoid DCs were more activated, and serum IgG and IFN-α were increased. In contrast, TLR7-deficient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG. These findings reveal opposing inflammatory and regulatory roles for TLR7 and TLR9, despite similar tissue expression and signaling pathways. These results have important implications for TLR-directed therapy of autoimmune disease. Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis in susceptible mice. We report that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag. TLR9 and TLR7 also had dramatic effects on clinical disease in lupus-prone mice. In the absence of TLR9, autoimmune disease was exacerbated, lymphocytes and plasmacytoid DCs were more activated, and serum IgG and IFN-alpha were increased. In contrast, TLR7-deficient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG. These findings reveal opposing inflammatory and regulatory roles for TLR7 and TLR9, despite similar tissue expression and signaling pathways. These results have important implications for TLR-directed therapy of autoimmune disease.Antibodies (Abs) to RNA- and DNA-containing autoantigens are characteristic of systemic lupus erythematosus (SLE). We showed previously that Toll-like receptor (TLR) 9, recognizing DNA, is required for the spontaneous generation of DNA autoantibodies, but not for the development of lupus nephritis in susceptible mice. We report that lupus-prone mice deficient in TLR7, a receptor for ssRNA, failed to generate Abs to RNA-containing antigens (Ags) such as Smith (Sm) Ag. TLR9 and TLR7 also had dramatic effects on clinical disease in lupus-prone mice. In the absence of TLR9, autoimmune disease was exacerbated, lymphocytes and plasmacytoid DCs were more activated, and serum IgG and IFN-alpha were increased. In contrast, TLR7-deficient mice had ameliorated disease, decreased lymphocyte activation, and decreased serum IgG. These findings reveal opposing inflammatory and regulatory roles for TLR7 and TLR9, despite similar tissue expression and signaling pathways. These results have important implications for TLR-directed therapy of autoimmune disease. |
| Author | Shlomchik, Mark J. Kashgarian, Michael Nickerson, Kevin Shupe, Jonathan Flavell, Richard A. Christensen, Sean R. |
| Author_xml | – sequence: 1 givenname: Sean R. surname: Christensen fullname: Christensen, Sean R. organization: Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510 – sequence: 2 givenname: Jonathan surname: Shupe fullname: Shupe, Jonathan organization: Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06510 – sequence: 3 givenname: Kevin surname: Nickerson fullname: Nickerson, Kevin organization: Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06510 – sequence: 4 givenname: Michael surname: Kashgarian fullname: Kashgarian, Michael organization: Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510 – sequence: 5 givenname: Richard A. surname: Flavell fullname: Flavell, Richard A. organization: Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510 – sequence: 6 givenname: Mark J. surname: Shlomchik fullname: Shlomchik, Mark J. email: mark.shlomchik@yale.edu organization: Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06510 |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16973389$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Antibody Specificity Autoantibodies - biosynthesis Autoimmune diseases CELLIMMUNO Cells, Cultured Deoxyribonucleic acid Dilution DNA Female Humans HUMDISEASE Immune system Immunoglobulin G - blood Lupus Lupus Erythematosus, Systemic - immunology Lupus Erythematosus, Systemic - metabolism Lupus Erythematosus, Systemic - pathology Lymphocyte Activation - immunology Male Mice Mice, Inbred C57BL Mice, Inbred MRL lpr Mice, Knockout MOLIMMUNO Mortality Rodents Studies Toll-Like Receptor 7 - deficiency Toll-Like Receptor 7 - genetics Toll-Like Receptor 7 - physiology Toll-Like Receptor 9 - deficiency Toll-Like Receptor 9 - genetics Toll-Like Receptor 9 - physiology |
| Title | Toll-like Receptor 7 and TLR9 Dictate Autoantibody Specificity and Have Opposing Inflammatory and Regulatory Roles in a Murine Model of Lupus |
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