Table 2.
Summary of recent immunomics applications and their impact on our understanding of pediatric rheumatic disease (II).
| Immunomics techniques | Clinical application and discovery | References |
|---|---|---|
| Transcriptomics | ||
| Microarrays | cSLE disease activity and realization of innate immunity as part of immunopathogenesis | |
| Type I interferon signature and type I interferon-inducible gene expression | (38–40) | |
| JIA pathogenesis and treatment | ||
| Dysregulated interleukin-1 pathway in sJIA with active disease, anti-IL 1 therapies were introduced with good outcomes | (41–45) | |
| Differences in PBMC transcriptomics profiles – subtype-specific and/or disease state-specific in sJIA and non-sJIA | (39, 46–50) | |
| Neutrophil-specific transcriptional abnormalities persist in polyarticular JIA irrespective of disease state, suggesting aberrations in neutrophil metabolism | (51, 52) | |
| Kawasaki disease diagnosis | ||
| Whole blood gene expression signature – separates the disease from other childhood febrile illnesses | (53) | |
| MicroRNA (miRNA) |
JDM disease activity | |
| Downregulation of miRNA-10a associated with increased expression of NF-kB-controlled inflammatory mediators | (54) | |
| RNA sequencing (RNA-seq) |
sJIA disease activity | |
| NK cell gene dysregulation (increased expression of innate genes S100A9 and TLR4, decreased expression of immune-regulating genes IL10RA and GZMK) in active disease | (55) | |
| JIA pathogenesis | ||
| Increased autophagy with up regulation of two key genes, fatty acid synthase (FASN) and carnitine palmitoyltransferase 1A (CPT1A) within the fatty acid synthesis pathway | (56, 57) | |
| JIA treatment response | ||
| Monocyte gene expression profile may predict methotrexate non-responders | (58) | |
JIA, Juvenile Idiopathic Arthritis; sJIA, systemic JIA; JDM, Juvenile Dermatomyositis; PBMC, Peripheral Blood mononuclear Cells; SLE, Systemic Lupus Erythematosus; TLR, Toll-like receptor.