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Role of interferons in SLE

Bengtsson, Anders A. LU and Ro¨nnblom, Lars (2017) In Best Practice and Research: Clinical Rheumatology
Abstract

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects many different organ systems, with excessive production of type I interferons (IFNs) and autoantibodies against nucleic acids as hallmarks. Activation of the type I IFN system in SLE is due to continuous stimulation of plasmacytoid dendritic cells by endogenous nucleic acids, leading to sustained type I IFN production. This is reflected by an overexpression of type I IFN-regulated genes or an IFN signature. Type I IFNs have effects on both the innate and adaptive immune systems, which contribute to both loss of tolerance and the autoimmune disease process. In this review, we discuss the current understanding of IFNs in SLE, focusing on their... (More)

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects many different organ systems, with excessive production of type I interferons (IFNs) and autoantibodies against nucleic acids as hallmarks. Activation of the type I IFN system in SLE is due to continuous stimulation of plasmacytoid dendritic cells by endogenous nucleic acids, leading to sustained type I IFN production. This is reflected by an overexpression of type I IFN-regulated genes or an IFN signature. Type I IFNs have effects on both the innate and adaptive immune systems, which contribute to both loss of tolerance and the autoimmune disease process. In this review, we discuss the current understanding of IFNs in SLE, focusing on their regulation, the influence of genetic background, and environmental factors and therapies that are under development aiming to inhibit the type I IFN system in SLE.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Biologic therapy, Interferon type I, Lupus erythematosus, systemic, Plasmacytoid dendritic cell
in
Best Practice and Research: Clinical Rheumatology
publisher
Baillière Tindall
external identifiers
  • scopus:85032883977
ISSN
1521-6942
DOI
10.1016/j.berh.2017.10.003
language
English
LU publication?
yes
id
e4d203bb-f377-4f98-a74e-49b35da750f2
date added to LUP
2017-12-12 16:17:12
date last changed
2018-01-07 12:28:39
@article{e4d203bb-f377-4f98-a74e-49b35da750f2,
  abstract     = {<p>Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that affects many different organ systems, with excessive production of type I interferons (IFNs) and autoantibodies against nucleic acids as hallmarks. Activation of the type I IFN system in SLE is due to continuous stimulation of plasmacytoid dendritic cells by endogenous nucleic acids, leading to sustained type I IFN production. This is reflected by an overexpression of type I IFN-regulated genes or an IFN signature. Type I IFNs have effects on both the innate and adaptive immune systems, which contribute to both loss of tolerance and the autoimmune disease process. In this review, we discuss the current understanding of IFNs in SLE, focusing on their regulation, the influence of genetic background, and environmental factors and therapies that are under development aiming to inhibit the type I IFN system in SLE.</p>},
  author       = {Bengtsson, Anders A. and Ro¨nnblom, Lars},
  issn         = {1521-6942},
  keyword      = {Biologic therapy,Interferon type I,Lupus erythematosus, systemic,Plasmacytoid dendritic cell},
  language     = {eng},
  month        = {11},
  publisher    = {Baillière Tindall},
  series       = {Best Practice and Research: Clinical Rheumatology},
  title        = {Role of interferons in SLE},
  url          = {http://dx.doi.org/10.1016/j.berh.2017.10.003},
  year         = {2017},
}