期刊
IMMUNITY
卷 25, 期 3, 页码 383-392出版社
CELL PRESS
DOI: 10.1016/j.immuni.2006.08.010
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资金
- NATIONAL CANCER INSTITUTE [P01CA084512, R01CA078846] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI057234] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR046589] Funding Source: NIH RePORTER
- NCI NIH HHS [P01 CA084512, R01 CA078846] Funding Source: Medline
- NIAID NIH HHS [U19 AI057234-02] Funding Source: Medline
- NIAMS NIH HHS [R01 AR46589-01] Funding Source: Medline
Different genetic alterations may lead to type I interferon (IFN) overproduction in human systemic lupus erythematosus (SLE). The increased bioavailability of type I IFN contributes to peripheral tolerance breakdown through the activation of immature myeloid dendritic cells (mDCs). IFN-matured mDCs activate autoreactive T cells. These cells, together with plasmacytoid DCs, help expand autoreactive B cells. IFN-matured DCs also activate cytotoxic CD8(+) T cells, possibly increasing apoptotic cell availability. The capture of apoptotic cells by mDCs and of nucleic acid-containing immune complexes by plasmacytoid DCs and B cells amplifies the autoimmune reaction leading to disease manifestations. Genetic alterations in lineages other than B cells might explain other autoimmune syndromes where type I IFNs appear to be involved.
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