Related Experiment Video
Updated: Jun 23, 2026

Detecting Migration and Infiltration of Neutrophils in Mice
Published on: February 6, 2020
Gene expression profiling in neutrophils from children with polyarticular juvenile idiopathic arthritis
James N Jarvis1, Kaiyu Jiang, Mark Barton Frank
1Pediatric Rheumatology Research, College of Medicine, Children's Hospital of Oklahoma, University of Oklahoma, Oklahoma City, OK 73013, USA. james-jarvis@ouhsc.edu
Insights
Neutrophil gene expression abnormalities persist in children with polyarticular juvenile idiopathic arthritis (JIA) even in remission. This suggests a complex interplay between innate and adaptive immunity in JIA pathogenesis.
Area of Science:
- Immunology
- Genetics
- Pediatrics
Background:
- Previous studies reported neutrophil activation defects in polyarticular juvenile idiopathic arthritis (JIA).
- The persistence of these abnormalities during remission and the underlying pathways were not fully understood.
Purpose of the Study:
- To determine if gene expression abnormalities in neutrophils persist in children with polyarticular JIA during remission.
- To utilize systems biology to elucidate the pathological pathways in polyarticular JIA.
Main Methods:
- Gene expression profiling was conducted on neutrophils from children with polyarticular JIA.
- Participants were categorized into active disease, clinical remission with medication (CRM), and clinical remission without medication (CR) groups.
- A control group of healthy children was included for comparison.
Main Results:
- Neutrophil abnormalities were observed in polyarticular JIA patients even after achieving disease remission.
- No significant differences in specific gene expression were found between active disease and CRM groups, though cluster analysis showed separation.
- Comparison of CR status patients with healthy controls revealed pro- and anti-inflammatory gene networks, indicating a homeostatic balance rather than a return to normal immune function.
- Gene overexpression in CR status patients supports a role for neutrophils in regulating adaptive immunity in JIA.
Conclusions:
- Neutrophil gene profiling in polyarticular JIA highlights their significant role in disease pathogenesis.
- The findings suggest intricate interactions between innate and adaptive immunity in JIA, challenging conventional linear models.
Objective:
We have previously reported a defect in neutrophil activation in children with polyarticular juvenile idiopathic arthritis (JIA). The current study was undertaken to determine whether gene expression abnormalities persist in JIA in remission and to use systems biology analysis to elucidate pathologic pathways in polyarticular JIA.
Methods:
We performed gene expression profiling on neutrophils from children with polyarticular JIA. Children were grouped according to disease status. We studied 14 children with active disease who were taking medication, 8 children with clinical remission of disease who were taking medication (CRM status), and 6 children with clinical remission of disease who were not taking medication (CR status). We also studied 13 healthy children whose age ranges overlapped those of the patients.
Results:
Neutrophil abnormalities persisted in children with polyarticular JIA even after disease remission was achieved. Children with active disease and those with CRM status showed no differences in expression of specific genes, although they could be separated on cluster analysis. A comparison of children with CR status and healthy control children revealed networks of pro- and antiinflammatory genes that suggested that remission is a state of homeostasis and balance rather than a return to normal immune function. Furthermore, gene overexpression in patients with CR status supports the hypothesis that neutrophils play a role in regulating adaptive immunity in this disease.
Conclusion:
Neutrophil gene profiling in polyarticular JIA suggests important roles for neutrophils in disease pathogenesis. These findings suggest the presence of complex interactions between innate and adaptive immunity, that are not easily modeled in conventional, linear, reductionist systems.