Emerging roles of TLR7 and TLR9 in murine SLE |
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| Affiliation: | 1. Department of Internal Medicine, Zabol University of Medical Sciences, Zabol, Iran;2. Zabol Medicinal Plant Research Center, Zabol University of Medical Sciences, Zabol, Iran;3. Kerman University of Medical Sciences, Kerman, Iran;4. Baqiyatollah Research Center for Gastroenterology and Liver Diseases, Baqiyatollah University of Medical Sciences, Tehran, Iran;5. Department of Laboratory Sciences, Faculty of Paramedicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran;6. School of Natural Sciences, Eskitis Institute for Drug Discovery, Griffith University, Nathan, Queensland, Australia;1. Immunology Laboratory, Department of Zoology, University of Calcutta, 35, Ballygunge Circular Road, Kolkata 700019, India;2. Basic and Clinical Immunology of Parasitic Diseases, Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019, UMR 8204, CIIL - Centre of Infection and Immunity Lille, F-59000 Lille, 1 rue du Professeur Calmette, 59019 Lille, France;1. Shanghai TB Key Laboratory, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China;2. Department of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China;3. Clinical Translational Research Center, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China;4. Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany |
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| Abstract: | Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by B cell hyperactivity leading to the production of various autoantibodies and subsequent development of glomerulonephritis, i.e. lupus nephritis. Among the principal targets of autoantibodies produced in murine SLE are nucleic acid–protein complexes, such as chromatin and ribonucleoproteins, and the envelope glycoprotein gp70 of endogenous retroviruses. The preferential production of these autoantibodies is apparently promoted by the presence of genetic abnormalities leading to defects in the elimination of apoptotic cells and to an enhanced expression of endogenous retroviruses. Moreover, recent studies revealed that the innate receptors TLR7 and TLR9 are critically involved in the activation of dendritic cells and autoreactive B cells through the recognition of endogenous DNA- or RNA-containing antigens and subsequent development of autoimmune responses against nuclear autoantigens. Furthermore, the regulation of autoimmune responses against endogenous retroviral gp70 by TLR7 suggested the implication of endogenous retroviruses in this autoimmune response. Clearly, further elucidation of the precise molecular role of TLR7 and TLR9 in the development of autoimmune responses will help to develop novel therapeutic strategies and targets for SLE. |
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