UNIGE document Scientific Article
previous document  unige:33448  next document
add to browser collection

TLR7 signaling exacerbates CNS autoimmunity through downregulation of Foxp3(+) Treg cells

Lalive, PH
Published in European Journal of Immunology. 2014, vol. 44, no. 1, p. 46-57
Abstract The innate Toll-like receptor 7 (TLR7) detects infections by recognizing viral and bacterial single-stranded RNA. In addition to pathogen-derived RNA, immune cells expressing high levels of TLR7, such as B cells and dendritic cells (DCs), can be activated by self-RNA. During myelin-induced experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, TLR7 expression is increased within the central nervous system (CNS). To define the contribution of TLR7 to the development of EAE, we evaluated the course of the disease in C57BL/6-Tlr7-deficient mice compared with that in WT mice and found that TLR7-deficient mice had decreased disease severity. This protection was associated with decreased myelin oligodendrocyte glycoprotein-specific T-cell activation by primed DCs, decreased circulating autoantibodies, attenuated inflammation within the CNS, and increased Foxp3(+) regulatory T cells in the periphery and in the CNS. In conclusion, we show that TLR7 is involved in the maintenance of autoimmunity in the pathogenesis of EAE.
PMID: 24018482
Full text
Article (Accepted version) (1.2 MB) - document accessible for UNIGE members only Limited access to UNIGE
Research group La Sclérose en plaques (908)
(ISO format)
LALIVE, PH et al. TLR7 signaling exacerbates CNS autoimmunity through downregulation of Foxp3(+) Treg cells. In: European Journal of Immunology, 2014, vol. 44, n° 1, p. 46-57. doi: 10.1002/eji.201242985 https://archive-ouverte.unige.ch/unige:33448

489 hits

1 download


Deposited on : 2014-01-20

Export document
Format :
Citation style :