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Background In a previous study, we demonstrated excessive activation of neutrophils leading to high concentrations of S100A12, a member of the damage-associated molecular pattern molecules (DAMP), in systemic-onset juvenile idiopathic arthritis (SOJIA) which is not found in other inflammatory diseases. Binding to the Receptor for Advanced Glycation Endproducts (RAGE) has been shown but exact molecular mechanisms of S100A12 leading to pro-inflammatory responses in immune cells are still lacking.

pediatric rheumatology online journal

The Damage Associated Molecular Pattern (DAMP) molecule S100A12 induces pro-inflammatory responses in monocytes via innate immunity signalling pathways