Type I Interferons in the Pathogenesis and Treatment of Autoimmune Diseases
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Type I Interferons in the Pathogenesis and Treatment of Autoimmune Diseases Jiao Jiang 1,2 & Ming Zhao 1,2 & Christopher Chang 3,4 & Haijing Wu 1,2 & Qianjin Lu 1,2
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Type I interferons (IFN-Is) are a very important group of cytokines that are produced by innate immune cells but also act on adaptive immune cells. IFN-Is possess antiviral, antitumor, and anti-proliferative effects, as well are associated with the initiation and maintenance of autoimmune disorders. Studies have shown that aberrantly expressed IFN-Is and/or type I IFN-inducible gene signatures in the serum or tissues of patients with autoimmune disorders are linked to their pathogenesis, clinical manifestations, and disease activity. Type I interferonopathies with mutations in genes impacting the type I IFN signaling pathway have shown symptoms and characteristics similar to those of systemic lupus erythematosus (SLE). Furthermore, both interventions in animal models and clinical trials of therapies targeting the type I IFN signaling pathway have shown efficacy in the treatment of autoimmune diseases. Our review aims to summarize the functions and targeted therapies (as well as clinical trials) of IFN-Is in both adult and pediatric autoimmune diseases, such as SLE, pediatric SLE (pSLE), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), juvenile dermatomyositis (JDM), Sjögren syndrome (SjS), and systemic sclerosis (SSc), discussing the potential abnormal regulation of transcription factors and epigenetic modifications and providing a potential mechanism for pathogenesis and therapeutic strategies for future clinical use. Keywords Autoimmunedisease . TypeI interferonsignaling pathway . Epigenetic modifications . Systemiclupus erythematosus . Juvenile idiopathic arthritis . Sjogren’s syndrome . Interferonopathies
Abbreviations AGS Aicardi-Goutières syndrome BTK Bruton’s tyrosine kinase cGAS Cyclic GMP-AMP synthase IFN-I Type I interferon IRAK Interleukin-1 receptor-associated kinase
* Haijing Wu [email protected] * Qianjin Lu [email protected] 1
Department of Dermatology, Second Xiangya Hospital, Central South University, Changsha 410008, Hunan, People’s Republic of China
2
Hunan Key Laboratory of Medical Epigenomics, Second Xiangya Hospital, Central South University, Changsha 410008, Hunan, People’s Republic of China
3
Division of Pediatric Immunology and Allergy, Joe DiMaggio Children’s Hospital, Hollywood, FL 33021, USA
4
Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA 95616, USA
IRF ISG JAK JDM JIA MAVS MDA MyD pDC PRR pSjS pSLE RA RIG-I SSc STAT STING Syk TBK TLR TRAF TREX
Interferon regulatory family Interferon-stimulated gene Janus kinase Juvenile dermatomyositis Juvenile idiopathic arthritis Mitochondrial antiviral signaling protein Melanoma differentiation-associated gene Myeloid differentiation primary response gene Plasmacytoid dendritic cell Pattern recognition receptor primary Sjögren
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