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Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis
Bharati Matta1, Betsy J Barnes2
1Center for Autoimmune Musculoskeletal and Hematopoietic Diseases, Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, USA.
Cytokine
|May 28, 2019
Summary
Systemic lupus erythematosus (SLE) involves immune cells producing type I interferon (IFN). Genetic risk factors like IRF5 influence IFN production and autoantibodies in SLE patients.
Area of Science:
- Immunology
- Autoimmune Diseases
- Genetics
Background:
- Systemic lupus erythematosus (SLE) is a complex autoimmune disease impacting multiple organs.
- Type I interferon (IFN) gene signature and autoantibodies are key features of SLE.
- Plasmacytoid dendritic cells (pDCs) are primary type I IFN producers, with their activity modulated by other immune cells.
Purpose of the Study:
- To review immune cell types involved in type I IFN production and regulation in SLE.
- To discuss potential triggers for endogenous type I IFN production in SLE.
- To explore the impact of IRF5-SLE risk haplotypes on immune cell populations in SLE.
Main Methods:
- Literature review focusing on immune cell roles in type I IFN pathways in SLE.
- Analysis of genetic associations between IRF5 and SLE risk.
- Examination of autoantibody profiles and IFN activity in SLE patients.
Main Results:
- Elevated IFNα activity is observed in SLE patients with IRF5 risk polymorphisms and specific autoantibodies (anti-RBP, anti-dsDNA).
- Neutrophils and their extracellular traps (NETs) are implicated as sources of type I IFNs and autoantigens in SLE.
- Dysregulation of immune cells in SLE is potentially exacerbated by type I IFN exposure.
Conclusions:
- IRF5 genetic variants are linked to SLE pathogenesis and IFN dysregulation.
- Multiple immune cells, including pDCs and neutrophils, contribute to type I IFN production in SLE.
- Understanding these cellular interactions and IFN pathways is crucial for SLE management.
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