Journal
JOURNAL OF IMMUNOLOGY
Volume 192, Issue 12, Pages 5459-5468Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1002795
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Funding
- Mary Kirkland Center for Lupus Research, National Institutes of Health [AI059893]
- Alliance for Lupus Research
- Lupus Research Institute
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Investigations of patients with systemic lupus erythematosus have applied insights from studies of the innate immune response to define IFN-I, with IFN-alpha as the dominant mediator, as central to the pathogenesis of this prototype systemic autoimmune disease. Genetic association data identify regulators of nucleic acid degradation and components of TLR-independent, endosomal TLR-dependent, and IFN-I-signaling pathways as contributors to lupus disease susceptibility. Together with a gene expression signature characterized by IFN-I-induced gene transcripts in lupus blood and tissue, those data support the conclusion that many of the immunologic and pathologic features of this disease are a consequence of a persistent self-directed immune reaction driven by IFN-I and mimicking a sustained antivirus response. This expanding knowledge of the role of IFN-I and the innate immune response suggests candidate therapeutic targets that are being tested in lupus patients.
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