The many faces of type I interferon in systemic lupus erythematosus

Claudia Mauri, Madhvi Menon

Research output: Contribution to journalArticlepeer-review


Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with a broad spectrum of clinical presentations involving multiple organ systems. An abnormal response to self-antigens is thought to drive the development of SLE; however, the factors that underlie this dysfunction are not clear. In this issue of the JCI, Li and colleagues present compelling evidence to show that type I interferons (IFNs) produced by plasmacytoid dendritic cells inhibit the clearance of apoptotic cells (ACs) by marginal zone macrophages. Specifically, type I IFNs increase the translocation of marginal zone (MZ) B cells to the follicular region of the spleen, thereby disrupting interactions between these B cells and MZ macrophages (MZMs), which in turn disrupts megakaryoblastic leukemia 1-mediated (MKL1-mediated) mechanosensing and inhibits AC phagocytosis by MZMs. The results of this study provide important insight into factors that inhibit AC clearance and promote the development of SLE.

Original languageEnglish
Pages (from-to)2562-4
Number of pages3
JournalThe Journal of clinical investigation
Issue number7
Publication statusPublished - 1 Jul 2015


  • Animals
  • Apoptosis/immunology
  • Female
  • Humans
  • Interferon Type I/immunology
  • Lupus Erythematosus, Systemic/immunology
  • Mechanotransduction, Cellular/immunology


Dive into the research topics of 'The many faces of type I interferon in systemic lupus erythematosus'. Together they form a unique fingerprint.

Cite this