期刊
JOURNAL OF IMMUNOLOGY
卷 197, 期 4, 页码 1447-1459出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1600624
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资金
- National Institutes of Health Research (NIHR) [CS-2013-13-032] Funding Source: National Institutes of Health Research (NIHR)
- Cancer Research UK [17723] Funding Source: researchfish
- National Institute for Health Research [CS-2013-13-032] Funding Source: researchfish
- The Francis Crick Institute
- Cancer Research UK [10066] Funding Source: researchfish
Plasma cells (PCs) as effectors of humoral immunity produce Igs to match pathogenic insult. Emerging data suggest more diverse roles exist for PCs as regulators of immune and inflammatory responses via secretion of factors other than Igs. The extent to which such responses are preprogrammed in B-lineage cells or can be induced in PCs by the microenvironment is unknown. In this study, we dissect the impact of IFNs on the regulatory networks of human PCs. We show that core PC programs are unaffected, whereas PCs respond to IFNs with distinctive transcriptional responses. The IFN-stimulated gene 15 (ISG15) system emerges as a major transcriptional output induced in a sustained fashion by IFN-alpha in PCs and linked both to intracellular conjugation and ISG15 secretion. This leads to the identification of ISG15-secreting plasmablasts/PCs in patients with active systemic lupus erythematosus. Thus, ISG15-secreting PCs represent a distinct proinflammatory PC subset providing an Ig-independent mechanism of PC action in human autoimmunity.
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