Study summary · research use only
Cathelicidin LL-37: A new important molecule in the pathophysiology of systemic lupus erythematosus
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This narrative review discusses the antimicrobial peptide cathelicidin LL-37 and its proposed role in the pathophysiology of systemic lupus erythematosus (SLE) in humans. LL-37 is described as produced by epithelial cells, neutrophils, and lymphocytes as antimicrobial defense, and beyond this it can act as an immunomodulator linked to autoimmune disease. LL-37 can form complexes with DNA that stimulate plasmacytoid dendritic cells (pDCs) to produce type I interferon (IFN) via recognition by the FcgammaRII receptor and TLR9 signaling, described as contributing to early autoimmunity in SLE patients. The review covers LL-37's structure, function, and reported importance in innate immunity and SLE, concluding it is an important molecule in SLE pathophysiology mainly via increased pDC-derived IFN, and suggesting it could serve as a disease biomarker.
Abstract
Cathelicidin LL-37 is an antimicrobial peptide that is synthesized by epithelial cells, neutrophils, or lymphocytes and act as an essential defense mechanism against bacterial, viral, or fungi infection of eukaryotic organisms. However, in recent years, this cathelicidin has gained the interest of the scientific community because, besides its antimicrobial properties, LL-37 is an immunomodulator that can contribute to the development of autoimmune diseases. The other non-antimicrobial function of this cathelicidin is its ability to form complexes with the DNA, stimulating plasmacytoid dendritic cells (pDCs) to produce type I IFN, deciding the course of autoimmune diseases, including systemic lupus erythematosus (SLE). The chronic activation of pDCs by surrounding complexes is a crucial factor for the early development of autoimmunity in SLE patients. This stimulation is given by the complexes (LL-37-DNA/anti-DNA) recognized by the receptor FcγRII on pDCs, allowing its endocytosis and its recognition via TLR9, leading to the activation of pDCs and enhanced type I IFN production. In this article, we reviewed the structure, function, and importance of LL-37 in innate immunity, as well as its biological plausibility in the pathophysiology of autoimmune diseases such as SLE. In this narrative review, we included primary journal articles describing the function, structure, prevalence, and importance of LL-37 in various manifestations of SLE, as well as LL-37 and anti-LL37 antibodies in patients with SLE or other autoimmune diseases. In conclusion, LL-37 is an essential molecule in the pathophysiology of SLE, mainly by its role in increasing the production of IFN by pDCs, which postulates it as a crucial molecule in the pathophysiology of SLE and, given plausibility biology, could serve as a biomarker of the disease.
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