Fig. 1

The NLRP3 inflammasome pathway. Here the role of MYD88 as a downstream adaptor molecule in the toll-like receptors and IL-1 receptors is shown in the NLRP3 inflammasome pathway. It has already been proven that MYD88 can cause an induction of NF-κβ which is of importance for the survival of Waldenström’s macroglobulinemia cells. MYD88 serves however hypothetically as a mutual factor in the pathophysiology of MGUS or WD and Schnitzler’s syndrome due to its relation with NF-κβ, NLRP3 and the inflammasome. Furthermore, the increased activity of the inflammasome as seen in Schnitzler’s syndrome might theoretically – via IL1-receptors and MYD88 - increase the dysregulation in the NF-κβ pathway influencing the MGUS or WD