Abstract
Interferon-α plays a crucial role in the pathogenesis of systemic lupus erythematosus. Nevertheless, the different human cell types producing this cytokine as well as the stimuli inducing its production have not been completely characterized. So far, a subpopulation of dendritic cells activated by immune complexes has been identified as major producers of interferon-α in patients with lupus. However, those cells represent a minor population and some studies have reported the secretion of interferon-α by other cells. On the other hand, more than 50% of blood leukocytes are neutrophils and their functions are still not fully understood. Recent data suggest that neutrophils, though usually not considered interferon-α-producing cells, may represent an unexpected source of this cytokine in response to some lupus stimuli.
Highlights
Interferon-α plays a crucial role in the pathogenesis of systemic lupus erythematosus
A recent study confirmed the latter observation by using polymorphonuclear leukocyte (PMN) isolated from patients with systemic lupus erythematosus (SLE) and described the induction of type I IFN upon activation with granulocyte colony-stimulating factor (G-CSF), phorbol 12-myristate 13-acetate (PMA), or transfected poly I:C, the natural lupus stimulus and the mechanism involved were not identified [14]
Together with our previous results showing that free chromatin stimulates PMNs [16] independently of TLR9 [17], leading to interleukin (IL)-8, IL-6, and tumor necrosis factor (TNF) secretion, CD11b upregulation, and increased phagocytic activity, all of those studies reveal an unsuspected role for PMNs in SLE pathogenesis
Summary
Interferon-α plays a crucial role in the pathogenesis of systemic lupus erythematosus. The involvement of IFN-α in SLE development is further supported by the IFN-inducible gene expression signature that characterizes a clinical subset of patients with SLE and more severe disease (for example, damage of the kidneys or the central nervous system) [3].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
