Association of CCL2 with systemic inflammation in Schnitzler syndrome

Abstract

This summary relates to https://doi.

CCL 2 serves as a downstream effector of interleukin‐1β and tumour necrosis factor‐α signalling in Schnitzler syndrome

“…However, in the study by Krause et al . in this issue of the BJD , the authors failed to demonstrate a correlation between the CCL2 level and disease duration, neutrophilia, skin disease or gammopathy . If CCL2 has good potential for mediator release from basophils and mast cells, and if mast cells are the major cell source of IL‐1β, CCL2 may play a role in inducing skin eruptions.…”

“…Bone alterations are another characteristic feature of Schnitzler syndrome, with osteosclerosis leading to clinically evident tibial and/or pelvic bone pain . The current issue of the BJD presents interesting clinical research regarding chemokine (C‐C motif) ligand 2 (CCL2), a chemoattractant for monocytes but not neutrophils, in Schnitzler syndrome . The correlations of the serum CCL2 level with global disease activity, particularly bone pain, and early treatment response highlighted its critical role in the pathogenetic cascade contributing to bone remodelling in Schnitzler syndrome .…”

“…The current issue of the BJD presents interesting clinical research regarding chemokine (C‐C motif) ligand 2 (CCL2), a chemoattractant for monocytes but not neutrophils, in Schnitzler syndrome . The correlations of the serum CCL2 level with global disease activity, particularly bone pain, and early treatment response highlighted its critical role in the pathogenetic cascade contributing to bone remodelling in Schnitzler syndrome . The CCL2 level showed a rapid reduction as early as 1 week after initiation of effective anti‐IL‐1 therapy, suggesting IL‐1β directly induces CCL2 secretion from cells.…”

“…The correlations of the serum CCL2 level with global disease activity, particularly bone pain, and early treatment response highlighted its critical role in the pathogenetic cascade contributing to bone remodelling in Schnitzler syndrome . The CCL2 level showed a rapid reduction as early as 1 week after initiation of effective anti‐IL‐1 therapy, suggesting IL‐1β directly induces CCL2 secretion from cells. In ex vivo experiments, mononuclear cells and fibroblasts were identified as producers of CCL2, along with IL‐1β and tumour necrosis factor (TNF)‐α, the blood levels of which were correlated with that of CCL2 in Schnitzler syndrome …”

“…The CCL2 level showed a rapid reduction as early as 1 week after initiation of effective anti‐IL‐1 therapy, suggesting IL‐1β directly induces CCL2 secretion from cells. In ex vivo experiments, mononuclear cells and fibroblasts were identified as producers of CCL2, along with IL‐1β and tumour necrosis factor (TNF)‐α, the blood levels of which were correlated with that of CCL2 in Schnitzler syndrome …”