期刊
CURRENT OPINION IN IMMUNOLOGY
卷 18, 期 6, 页码 676-682出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2006.09.014
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资金
- NCI NIH HHS [R01 CA078846, P01 CA084512] Funding Source: Medline
- NIAMS NIH HHS [R01 AR46589-01] Funding Source: Medline
- PHS HHS [U19 AIO57234-02] Funding Source: Medline
In recent years, the study of systemic lupus erythematosus (SLE) patients has revealed a central role for type I interferon (IFN) in disease pathogenesis. IFN induces the unabated activation of peripheral dendritic cells, which select and activate autoreactive T cells rather than deleting them, thus failing to induce peripheral tolerance. IFN also directly affects T cells and B cells. Furthermore, immune complexes binding to Fc gamma R and Toll-like receptors provide an amplification loop for IFN production and B-cell activation in SLE. Polymorphisms in genes that control IFN production or its downstream signaling pathway, such as IRF5, might be responsible for some of these alterations. This novel information is leading to the development of IFN antagonists as a potential therapeutic intervention in SLE, thus bringing hope to SLE patients.
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