AbstractPurpose of review
Systemic lupus erythematosus (SLE) pathogenesis is complex. Aberrancies of immune function that previously were described but not well understood are now becoming better characterized, in part through recognition of monogenic cases of lupus-like disease.Recent findings
We highlight here recent descriptions of metabolic dysfunction, cytokine dysregulation, signaling defects, and DNA damage pathways in SLE. Specifically, we review the effects of signaling abnormalities in mammalian target of rapamycin, Rho kinase, Bruton's tyrosine kinase, and Ras pathways. The importance of DNA damage sensing and repair pathways, and their influence on the overproduction of type I interferon in SLE are also reviewed.Summary
Recent findings in SLE pathogenesis expand on previous understandings of broad immune dysfunction. These findings have clinical applications, as the dysregulated pathways described here can be targeted by existing and preclinical therapies.