Juvenile dermatomyositis (JDM) is an autoimmune myositis that primarily causes inflammation of the skin and skeletal muscles in children [1]. The pathophysiology of JDM is heterogeneous, and previous studies have reported that the clinical manifestations and disease course vary depending on the presence of specific myositis-specific autoantibodies (MSAs) [[1], [2], [3]]. Although anti-transcriptional intermediary factor 1 gamma (TIF1γ) antibodies are associated with an increased risk of malignancy in adults, they are more frequently associated with severe skin involvement and a chronic disease course in pediatric cases. Additionally, patients with anti-melanoma differentiation–associated protein 5 (MDA5) antibodies exhibit a higher incidence of skin ulceration and are at increased risk of developing interstitial lung diseases (ILDs). Furthermore, patients with anti-nuclear matrix protein 2 (NXP2) antibody are more prone to severe muscle involvement and calcinosis [[1], [2], [3]]. Despite well-established associations between MSAs and clinical phenotypes, the underlying mechanisms remain inadequately elucidated, underscoring that further investigation into the disease pathogenesis is urgently needed.

Recent studies have emphasized the key contribution of cytokines in the pathogenesis of autoimmune diseases, and serum cytokines have been suggested to correlate with disease activity and clinical symptoms in JDM [2,[4], [5], [6], [7]]. In adult dermatomyositis, interferon (IFN) signaling has been implicated in disease pathogenesis; however, cytokine profile analyses in pediatric patients remain insufficient [[8], [9], [10]]. Considering these findings, elucidating the role of cytokines in JDM may both enhance our understanding of disease mechanisms and enable the discovery of novel biomarkers and therapeutic targets. This study aims to characterize serum cytokine profiles in patients with JDM and investigate their associations with MSA subgroups, clinical manifestations, and laboratory findings. Identifying unique inflammatory patterns in each MSA-positive subgroup can enhance our understanding of disease pathogenesis and contribute to the discovery of novel biomarkers for JDM.