Literature DB >> 30233083

Correction: Report of the inaugural Interferon Research Summit: interferon in inflammatory diseases.

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Abstract

[This corrects the article DOI: 10.1136/lupus-2018-000276.].

Entities:  

Year:  2018        PMID: 30233083      PMCID: PMC6135461          DOI: 10.1136/lupus-2018-000276corr1

Source DB:  PubMed          Journal:  Lupus Sci Med        ISSN: 2053-8790


Crow MK, Ronnblom L. Report of the inaugural Interferon Research Summit: interferon in inflammatory diseases. Lupus Science & Medicine 2018;5:e000276. doi: 10.1136/lupus-2018-000276 The authors want to alert readers to the following two errors identified in the published version. At page 4 (column 1, 2nd sentence of last paragraph), the sentence should read as: “Young women (35–44 years) with SLE have a 50-fold increased risk of vascular complications…” In Table 1, the row under the drug “Anifrolumab” states that the drug is at Phase II for Sjögren’s syndrome. This has been stated incorrectly and has been removed. The updated Table 1 is now available below: Therapeutic agents targeting components of the type I IFN pathway and in clinical development for IFN-driven diseases *Development status unknown. †European Medicines Agency approved for rheumatoid arthritis. IFN, interferon; IFNAR1, type I interferon alpha receptor subunit 1; ILT7, immunoglobulin-like transcript 7; JAK, Janus kinase; MOA, mechanism of action; pDCs, plasmacytoid dendritic cell. In the legend of figure 1, the term ‘interferon-stimulating genes’ appears. The correct term is ‘interferon-stimulated genes’. The role of IFN in viral infection over time. cDC, conventional dendritic cell; IFN, interferon; IL, interleukin; ISG, interferon-stimulated genes; pDC, plasmacytoid dendritic cells; PD-L1, programmed death ligand 1; PRR, pattern recognition receptor. Left panel adapted from Crouse J et al 9; right panel adapted from Zuniga EI et al 10 (Reprinted by permission from Springer Customer Service Centre GmbH: Springer Nature, Nature Reviews Immunology; Regulation of antiviral T cell responses by type I interferons. Crouse J, Kalinke U, Oxenius A, © 2015. Republished with permission of Annual Reviews, from Innate and Adaptive Immune Regulation During Chronic Viral Infections, Zuniga EI, Macal M, Lewis GM, et al, Vol. 2, © 2015; permission conveyed through Copyright Clearance Center).
Table 1

Therapeutic agents targeting components of the type I IFN pathway and in clinical development for IFN-driven diseases

DrugDrug MOADevelopment statusDisease
RSLV132RNA hydrolysisPhase IISystemic lupus erythematosus Sjögren's syndrome
SM101Anti–immune complexPhase IISystemic lupus erythematosusLupus nephritis
BIIB059Anti-BDCA2 (pDCs)Phase IISystemic lupus erythematosus
MEDI-7734Anti-ILT7 (pDCs)Phase IDermatomyositis Polymyositis Systemic sclerosis Sjögren's syndrome Systemic lupus erythematosus
JNJ-55920839Anti–IFN-α/ωPhase ISystemic lupus erythematosus
AGS-009Anti–IFN-αPhase I*Systemic lupus erythematosus
IFN-α-kinoidAnti–IFN-αPhase IIDermatomyositis
Phase IISystemic lupus erythematosus
AnifrolumabAnti-IFNAR1Phase IILupus nephritis
Phase IIISystemic lupus erythematosus
Baricitinib†JAK1/JAK2 inhibitorPhase IISystemic lupus erythematosus
PF-04965842JAK1 inhibitorPhase IISystemic lupus erythematosus

*Development status unknown.

†European Medicines Agency approved for rheumatoid arthritis.

IFN, interferon; IFNAR1, type I interferon alpha receptor subunit 1; ILT7, immunoglobulin-like transcript 7; JAK, Janus kinase; MOA, mechanism of action; pDCs, plasmacytoid dendritic cell.

  2 in total

Review 1.  The Genetic Association of IFN-λs with Human Inflammatory Disorders Remains a Conundrum.

Authors:  Sreedhar Chinnaswamy; Marek L Kowalski
Journal:  J Interferon Cytokine Res       Date:  2019-06-04       Impact factor: 2.607

Review 2.  Type I interferon antagonists in clinical development for lupus.

Authors:  Jacqueline L Paredes; Timothy B Niewold
Journal:  Expert Opin Investig Drugs       Date:  2020-09-01       Impact factor: 6.206

  2 in total

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