The majority of patients with systemic lupus erythematosus (SLE) have high expression of
type I IFN-stimulated genes. Mitochondrial abnormalities have also been reported, but the …

Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus
erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal …

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 …

We formulate a two-phase paradigm of autoimmunity associated with systemic lupus
erythematosus, the archetypal autoimmune disease. The initial Toll-like receptor (TLR) …

Dysregulation of type I interferons (IFNs) has been implicated in the pathogenesis of
systemic lupus erythematosus (SLE) since the late 1970s. The majority of SLE patients …

Autoantibodies against nucleic acids and excessive type I interferon (IFN) are hallmarks of
human systemic lupus erythematosus (SLE). We previously reported that SLE neutrophils …

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 …

As demonstrated in the murine studies of persistent virus infection accompanied by
sustained production of IFN-I, blockade of the IFN-I pathway may reverse the immune …

Abstract Excess type I IFNs (IFN-I) have been linked to the pathogenesis of systemic lupus
erythematosus (SLE). Therapeutic use of IFN-I can trigger the onset of SLE and most lupus …

The central pathogenetic role of type I interferons (IFNs) in several systemic autoimmune
diseases is well established. Recent studies have also discovered a similar crucial role of …