Journal
EXPERT REVIEW OF CLINICAL IMMUNOLOGY
Volume 9, Issue 3, Pages 201-210Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1586/ECI.12.106
Keywords
anti-interferon therapy; autoimmune disease; innate immune activation; interferon induction; lupus model; nucleic acids; plasmacytoid dendritic cells; systemic lupus erythematosus; Toll-like receptor; type I interferon
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Funding
- NIH [AI074809]
- University of Texas MD Anderson Cancer Center Institutional Research Grant Program
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In recent years, active research using genomic, cellular and animal modeling approaches has revealed the fundamental forces driving the development of autoimmune diseases. Type I interferon imprints unique molecular signatures in a list of autoimmune diseases. Interferon is induced by diverse nucleic acid-containing complexes, which trigger innate immune activation of plasmacytoid dendritic cells. Interferon primes, activates or differentiates various leukocyte populations to promote autoimmunity. Accordingly, interferon signaling is essential for the initiation and/or progression of lupus in several experimental models. However, the heterogeneous nature of systemic lupus erythematosus requires better characterization on how interferon pathways are activated and subsequently promote the advancement of autoimmune diseases. Given the central role of type I interferon, various strategies are devised to target these cytokines or related pathways to curtail the progression of autoimmune diseases.
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