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Network Analysis Identifies Proinflammatory Plasma Cell Polarization for Secretion of ISG15 in Human Autoimmunity
Matthew A Care1, Sophie J Stephenson2, Nicholas A Barnes2
1Section of Experimental Haematology, Leeds Institute of Cancer and Pathology, University of Leeds, Leeds LS9 7TF, United Kingdom; Bioinformatics Group, Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom;
Interferons (IFNs) induce a distinct response in plasma cells (PCs), leading to the secretion of IFN-stimulated gene 15 (ISG15). This ISG15-secreting PC subset may drive inflammation in autoimmune diseases like lupus.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmunity
Background:
- Plasma cells (PCs) are key for antibody production but may have other immune regulatory roles.
- The influence of the microenvironment, such as interferons (IFNs), on PC function beyond antibody secretion is not fully understood.
Purpose of the Study:
- To investigate the impact of IFNs on the regulatory networks of human plasma cells.
- To identify novel functions and secreted factors of plasma cells.
Main Methods:
- Transcriptional profiling of human plasma cells treated with IFNs.
- Analysis of IFN-stimulated gene 15 (ISG15) expression and secretion.
- Identification of ISG15-secreting cells in patients with systemic lupus erythematosus.
Main Results:
- Core plasma cell programs remain unchanged by IFNs, but distinct transcriptional responses are observed.
- IFN-alpha induces sustained expression and secretion of ISG15 in plasma cells.
- A subset of ISG15-secreting plasmablasts/PCs is identified in patients with active systemic lupus erythematosus.
Conclusions:
- Interferons induce specific transcriptional changes in plasma cells, including the ISG15 system.
- ISG15-secreting plasma cells represent a novel proinflammatory subset.
- This Ig-independent mechanism highlights a new pathway for plasma cell involvement in human autoimmunity.
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