Type I interferon in systemic lupus erythematosus and other autoimmune diseases.

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

Immunity

journal_title

Immunity

authors

Banchereau J,Pascual V

doi

10.1016/j.immuni.2006.08.010

subject

Has Abstract

pub_date

2006-09-01 00:00:00

pages

383-92

issue

3

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(06)00395-5

journal_volume

25

pub_type

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