Researchers unravel how vitamin D shuts down inflammation in psoriasis
Munich/Kiel/La Jolla – A German-US research team has unravelled how vitamin D in conjunction with UV-B rays help reduce the chronic infection observed in patients with psoriasis (Science Translational Medicine 3(82): 82ra38). Typically, psoriasis occurs when the immune system sends out false danger signals that activate protein complexes called inflammasomes and ramp up the body’s inflammatory response to damage, leading to dry patches and the build up of dead skin cell plaques. When comparing gene expression in healthy and diseased skin biopsies, Jürgen Schauber and colleagues found that sensor protein AIM2, which recognises cytosolic DNA, was over expressed in the skin of psoriasis patients. AIM2 works with other proteins to assemble the inflammasome. The inflammasome then activates the cytokine Interleukin-1 beta, that in turn promotes inflammation. Yet this chain of events can be shut down by the antimicrobial peptide cathelicidin LL37 that can bind and neutralise cytosolic DNA. It turned out that vitamin D controls cathelicidin production in human skin and can foster the binding of cathelicidin LL37 to DNA. By ramping up the binding of cathelicidin to DNA, Vitamin D helps to prevent DNA from activating the AIM2 receptor and the inflammasome that triggers the autoimmune reaction. The authors suggest that cathelicidin may be a more specific target for therapy.