4.2 Article

Immunoprofiling of active and inactive systemic juvenile idiopathic arthritis reveals distinct biomarkers: a single-center study

期刊

PEDIATRIC RHEUMATOLOGY
卷 19, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12969-021-00660-9

关键词

Systemic juvenile idiopathic arthritis; Cytokines and inflammatory mediators; Inflammation; Proteomics; Ingenuity pathway analysis; High mobility group Box 1

资金

  1. Reumatikerforbundet
  2. Magnus Bergvalls stiftelse
  3. Ulla och Gustaf af Ugglas stiftelse
  4. Stiftelsen Samariten
  5. Karolinska Institutet foundations (KIK2HEH)
  6. Vetenskapsradet [2018-02885]
  7. region Stockholm [20190592]
  8. China Scholarship Council [201807930002]
  9. Karolinska Institute
  10. Swedish Research Council [2018-02885] Funding Source: Swedish Research Council

向作者/读者索取更多资源

This study identified a novel set of biomarkers that distinguish active sJIA from inactive sJIA or healthy controls, enabling a better understanding of the immune mechanisms at play in sJIA and aiding in the development of future diagnostic and therapeutic strategies.
Background This study aimed to perform an immunoprofiling of systemic juvenile idiopathic arthritis (sJIA) in order to define biomarkers of clinical use as well as reveal new immune mechanisms. Methods Immunoprofiling of plasma samples from a clinically well-described cohort consisting of 21 sJIA patients as well as 60 age and sex matched healthy controls, was performed by a highly sensitive proteomic immunoassay. Based on the biomarkers being significantly up- or down-regulated in cross-sectional and paired analysis, related canonical pathways and cellular functions were explored by Ingenuity Pathway Analysis (IPA). Results The well-studied sJIA biomarkers, IL6, IL18 and S100A12, were confirmed to be increased during active sJIA as compared to healthy controls. IL18 was the only factor found to be increased during inactive sJIA as compared to healthy controls. Novel factors, including CASP8, CCL23, CD6, CXCL1, CXCL11, CXCL5, EIF4EBP1, KITLG, MMP1, OSM, SIRT2, SULT1A1 and TNFSF11, were found to be differentially expressed in active and/or inactive sJIA and healthy controls. No significant pathway activation could be predicted based on the limited factor input to the IPA. High Mobility Group Box 1 (HMGB1), a damage associated molecular pattern being involved in a series of inflammatory diseases, was determined to be higher in active sJIA than inactive sJIA. Conclusions We could identify a novel set of biomarkers distinguishing active sJIA from inactive sJIA or healthy controls. Our findings enable a better understanding of the immune mechanisms active in sJIA and aid the development of future diagnostic and therapeutic strategies.

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