Please use this identifier to cite or link to this item:
|Title:||RNA sensing by conventional dendritic cells is central to the development of lupus nephritis||Authors:||Celhar, Teja
Thornhill, Susannah I.
De Magalhaes, Raquel
Jones, Leigh A.
Thamboo, Thomas P.
Zhou, Xin J.
Connolly, John E.
Wakeland, Edward K.
|Issue Date:||2015||Source:||Celhar, T., Hopkins, R., Thornhill, S. I., De Magalhaes, R., Hwang, S.-H., Lee, H.-Y., et al. (2015). RNA sensing by conventional dendritic cells is central to the development of lupus nephritis. Proceedings of the National Academy of Sciences, 112(45), 6195-6204.||Series/Report no.:||Proceedings of the National Academy of Sciences of the United States of America||Abstract:||Glomerulonephritis is a common and debilitating feature of systemic lupus erythematosus (SLE). The precise immune mechanisms that drive the progression from benign autoimmunity to glomerulonephritis are largely unknown. Previous investigations have shown that a moderate increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis. In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid dendritic cells (pDCs) slow progression; however, the critical cell that is responsible for driving full immunopathology remains unidentified. In this investigation we have shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7 model of SLE. We show that a novel expanding CD11b+ conventional DC subpopulation dominates the infiltrating renal inflammatory milieu, localizing to the glomeruli. Moreover, exposure of human myeloid DCs to IFN-α or Flu increases TLR7 expression, suggesting they may have a role in self-RNA recognition pathways in clinical disease. To our knowledge, this study is the first to highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine model of SLE.||URI:||https://hdl.handle.net/10356/81194
|DOI:||10.1073/pnas.1507052112||Rights:||© 2015 The Authors (Published by National Academy of Sciences).||Fulltext Permission:||none||Fulltext Availability:||No Fulltext|
|Appears in Collections:||SBS Journal Articles|
Updated on Jul 21, 2020
Updated on Mar 4, 2021
Updated on May 11, 2021
Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.