Abstract:
: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.
journal_name
Immunityjournal_title
Immunityauthors
Banchereau J,Pascual Vdoi
10.1016/j.immuni.2006.08.010subject
Has Abstractpub_date
2006-09-01 00:00:00pages
383-92issue
3eissn
1074-7613issn
1097-4180pii
S1074-7613(06)00395-5journal_volume
25pub_type
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