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Type I interferon receptor controls B-cell expression of nucleic acid-sensing Toll-like receptors and autoantibody production in a murine model of lupus.

Arthritis research & therapy | 2009

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of high-titer IgG autoantibodies directed against nuclear autoantigens. Type I interferon (IFN-I) has been shown to play a pathogenic role in this disease. In the current study, we characterized the role of the IFNAR2 chain of the type I IFN (IFN-I) receptor in the targeting of nucleic acid-associated autoantigens and in B-cell expression of the nucleic acid-sensing Toll-like receptors (TLRs), TLR7 and TLR9, in the pristane model of lupus.

Pubmed ID: 19624844 RIS Download

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Associated grants

  • Agency: NIAID NIH HHS, United States
    Id: T32 AI007290
  • Agency: NIAID NIH HHS, United States
    Id: F31 AI010663
  • Agency: NIAMS NIH HHS, United States
    Id: R21 AR049328
  • Agency: NIAID NIH HHS, United States
    Id: K08 AI080945
  • Agency: NIDDK NIH HHS, United States
    Id: U19 DK061934
  • Agency: NIAMS NIH HHS, United States
    Id: AR49328
  • Agency: NHLBI NIH HHS, United States
    Id: N01-HV-28183
  • Agency: NIAID NIH HHS, United States
    Id: AI-10663-02
  • Agency: NIAID NIH HHS, United States
    Id: AI50865
  • Agency: NIDDK NIH HHS, United States
    Id: U19 DK61934
  • Agency: NIAID NIH HHS, United States
    Id: AI50854
  • Agency: NHLBI NIH HHS, United States
    Id: N01HV28183

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BALB/cAnNCrl (tool)

RRID:MGI:2683685

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