Abstract
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 language | English |
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Pages (from-to) | 2562-4 |
Number of pages | 3 |
Journal | The Journal of clinical investigation |
Volume | 125 |
Issue number | 7 |
DOIs | |
Publication status | Published - 1 Jul 2015 |
Keywords
- Animals
- Apoptosis/immunology
- Female
- Humans
- Interferon Type I/immunology
- Lupus Erythematosus, Systemic/immunology
- Mechanotransduction, Cellular/immunology