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A cell type-specific transcriptomic approach to map B cell and monocyte type I interferon-linked pathogenic
Martina Severa1, Fabiana Rizzo1, Sundararajan Srinivasan2
1Department of Infectious Diseases, Istituto Superiore di Sanità, Rome, Italy.
Journal of Autoimmunity
|May 4, 2019
Summary
Dysregulation of the Interferon (IFN) system in Multiple Sclerosis (MS) impacts B cells and monocytes, leading to increased cell death and T cell migration, suggesting new therapeutic targets.
Area of Science:
- Immunology
- Neuroimmunology
- Molecular Biology
Background:
- The Interferon (IFN) system plays a crucial role in immune cell function, and its dysregulation is implicated in autoimmune diseases.
- Multiple Sclerosis (MS) is a chronic autoimmune disease affecting the central nervous system, with immune cells like B cells, monocytes, and T cells contributing to its pathogenesis.
Purpose of the Study:
- To investigate the role of endogenous Interferon (IFN) signaling and IFN-regulated pathways in the pathogenesis of Multiple Sclerosis (MS).
- To characterize the specific contributions of B cells and monocytes to MS development and maintenance through IFN-mediated mechanisms.
Main Methods:
- Utilized an Interferome-based, cell type-specific transcriptomic approach to analyze gene expression in B cells and monocytes from MS patients.
- Performed in-depth functional validation studies to assess cell death, signaling pathways (STAT-3/IL-16 axis), and antiviral responses.
- Investigated Epstein-Barr virus (EBV) infection control in MS B cells.
Main Results:
- Identified increased susceptibility to IFN-linked, caspase-3 dependent apoptosis in B cells and monocytes of MS patients, potentially due to chronic activation.
- Demonstrated that caspase-3 activation in MS monocytes influences the STAT-3/IL-16 axis, promoting IL-16 release and CD4+ T cell migration.
- Discovered a novel defect in type I IFN signaling and antiviral response pathways in MS B cells, impairing anti-viral defense and EBV control.
Conclusions:
- Endogenous IFN signaling and IFN-regulated cellular processes significantly contribute to MS pathogenesis by affecting B cell and monocyte function and fate.
- The findings highlight the pathogenic roles of IFN-mediated apoptosis, the STAT-3/IL-16 axis in monocytes, and impaired antiviral responses in B cells in MS.
- These insights into IFN-driven immune dysregulation in MS offer potential therapeutic strategies targeting specific cell types and pathways.
Keywords:
Antiviral stateApoptosisB cellInterferomeMonocyteRelapsing-remitting multiple sclerosisTranscriptomeType I interferon signalingMore Related Videos
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