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Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
Published on: June 14, 2018
Anti-interferon alpha treatment in SLE.
Kyriakos A Kirou1, Elena Gkrouzman
1Mary Kirkland Center for Lupus Research, Hospital for Special Surgery, Weill Cornell Medical College, 535 East 70th Street, New York, NY 10021, USA. kirouk@hss.edu
Clinical Immunology (Orlando, Fla.)
|April 10, 2013
Summary
Type I interferon (IFN-I) and plasmacytoid dendritic cells (pDCs) are key in systemic lupus erythematosus (SLE) pathogenesis. This review examines emerging therapies targeting these pathways, evaluating their pros and cons.
Area of Science:
- Immunology
- Rheumatology
- Molecular Biology
Background:
- Type I interferon (IFN-I) pathway, particularly interferon alpha (IFNα), is increasingly recognized for its role in systemic lupus erythematosus (SLE) pathogenesis.
- Plasmacytoid dendritic cells (pDCs) are identified as the primary producers of IFNα in SLE.
- This growing understanding has spurred the development of novel therapeutic strategies.
Purpose of the Study:
- To review the evidence supporting the pathogenic role of IFNα and pDCs in SLE.
- To provide an update on the current clinical development of therapies targeting these pathways.
- To discuss the potential benefits and drawbacks of different therapeutic approaches.
Main Methods:
- Literature review of studies investigating IFNα and pDC involvement in SLE.
- Analysis of clinical trial data for emerging IFNα-targeted therapies.
- Comparative assessment of treatment strategies including receptor blockade, IFNα neutralization, and pDC targeting.
Main Results:
- Substantial evidence links IFNα and pDCs to SLE pathogenesis.
- Several therapeutic strategies targeting IFNα and pDCs are in clinical trials, with some reaching Phase II.
- Different approaches, including direct IFNα blockade and pDC depletion, show promise but require further evaluation.
Conclusions:
- Targeting the IFNα pathway and pDCs represents a promising therapeutic avenue for SLE.
- Ongoing clinical trials will clarify the efficacy and safety of these novel treatments.
- Careful consideration of the advantages and disadvantages of each strategy is crucial for successful SLE management.
Keywords:
AEANAAPECEDB-cell activation factorBAFFBDCA2BILAG indexBritish Isles Lupus Assessment Group indexCCL2CXCL10Clinical trialDCDNAseIFc gamma receptor IIa, GC, glucocorticoidsFcγRIIaGMCSFGRIP1IFN-IIFN-regulated genesIFN-regulatory factorIFN-stimulated response elementIFNARIFNαIFNα KinoidIFNα receptorIFNα-KILILT7IRAKIRFIRGISREIVIgIg-like transcript 7Interferon alphaKLHMHCMajor Histocompatibility ComplexMyD88NETNFκBNKODNPBMCPDPI3KδPlasmacytoid dendritic cellsRBPRDBPCRNA binding proteinsRT-qPCRSAESCSLESLE response indexSRISTATSystemic lupus erythematosusT helper 1TLRTNF alpha-induced protein 3TNFAIP3TNIP1TRAFTYK2Th1Toll-like receptorsUVadverse event(s)antinuclear antibodiesautoimmune polyendocrinopathy candidiasis ectodermal dystrophyblood DC antigen 2chemokine (C–C) motif ligand 2chemokine (C–X–C) motif ligand 10dendritic celldeoxyribonuclease Idouble stranded DNAdsDNAglucocorticoid receptor-interacting protein 1granulocyte/macrophage colony-stimulating factorimmunoglobulininterferon alphainterleukininterleukin receptor associated kinaseintravenouslykeyhole limpet haemocyaninmAbmonoclonal antibodiesmyeloid differentiation factor 88natural killerneutrophil extracellular trapnuclear factor kappa BoligodeoxynucleotidespDCperipheral blood mononuclear cellspharmacodynamicphosphatidylinositol-3 kinase δplasmacytoid dendritic cellrandomized double-blind placebo controlledreal-time quantitative polymerase chain reactionserious adverse event (s)signal transducer and activator of transcriptionsubcutaneouslysystemic lupus erythematosustumor necrosis factor receptor-associated factortumor necrosis factor α-induced protein 3-interacting protein 1type I interferon(s)tyrosine kinase 2ultravioletMore Related Videos
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