Table 5.
Summary of recent immunomics applications and their impact on our understanding of pediatric rheumatic disease (V).
| Immunomics techniques | Clinical application and discovery | References |
|---|---|---|
| Cytomics | ||
| Multi-parametric flow cytometry | Childhood-onset SLE pathogenesis | |
| Impaired upregulation of PD-1 expression in monocytes and myeloid dendritic cells in active SLE patients as compared to healthy controls or SLE patients in remission, suggesting a possible mechanism in loss of peripheral tolerance | (112) | |
| Double negative T cell elevation (> 2.5%), in children with SLE, MCTD and ANA-positive JIA | (113) | |
| Mass cytometry (CyTOF) | JDM pathogenesis | |
| Defective phosphorylation of PLCγ2 in natural killer (NK) cells compared to healthy controls | (114) | |
| JIA pathogenesis | ||
| Treatment-naïve polyarticular JIA patients displayed enhanced IFN-γ signaling in CD4 T cells and monocytes. Naïve CD4 T cells had more strongly phosphorylated STAT1 and STAT3 as compared to monocytes, which displayed increased phosphorylation of STAT3 compared with controls. This suggests that attenuation of IFN-γ signaling could be a novel alternative therapy for polyarticular JIA. | (115) | |
| Childhood-onset SLE pathogenesis | ||
| Monocyte cytokine signatures with high monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein 1β (MIP1β) and interleukin-1 receptor antagonist (IL-1RA) were found in treatment-naïve SLE children | (116) | |
JIA, Juvenile Idiopathic Arthritis; SLE, Systemic Lupus Erythematosus.