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Published on: August 15, 2019
Chronic non-bacterial osteomyelitis and immune checkpoint molecules
Ummusen Kaya Akca1, Erdal Sag1,2, Busra Aydın2
1Division of Pediatric Rheumatology, Department of Pediatrics, Faculty of Medicine, Hacettepe University, Sihhiye Campus, 06100, Ankara, Turkey.
Plasma PD-1 levels were lower in pediatric chronic non-bacterial osteomyelitis (CNO) patients compared to controls. T cell exhaustion may not significantly contribute to CNO pathogenesis, suggesting immune checkpoints are linked to autoimmunity, not autoinflammation.
Area of Science:
- Immunology
- Pediatric Rheumatology
Background:
- Chronic non-bacterial osteomyelitis (CNO) is a pediatric autoinflammatory disease.
- Immune checkpoint molecules like TIM-3 and PD-1 play critical roles in regulating T cell responses.
- Understanding their role in CNO is crucial for elucidating disease mechanisms.
Purpose of the Study:
- To investigate plasma levels and cell surface expression of TIM-3 and PD-1 in pediatric CNO patients.
- To compare these levels and expression between CNO patients and healthy controls.
- To explore the potential role of T cell exhaustion in CNO pathogenesis.
Main Methods:
- Plasma samples and peripheral blood mononuclear cells were collected from CNO patients and healthy controls.
- Sandwich ELISA was used to measure plasma levels of TIM-3 and PD-1.
- Flow cytometry analyzed the cellular expression of PD-1 and TIM-3 on CD3+CD4+ T cells.
Main Results:
- Median plasma PD-1 levels were significantly lower in CNO patients compared to healthy controls (p=0.011).
- No significant differences were observed in plasma TIM-3 levels between groups (p=0.981).
- Cellular expression of PD-1 and TIM-3 on T cells did not differ significantly between CNO patients and controls.
Conclusions:
- Lower plasma PD-1 levels in CNO patients suggest a potentially distinct immune profile.
- The lack of difference in cellular expression of PD-1 and TIM-3 indicates T cell exhaustion might not be a major factor in CNO.
- Further research is warranted to differentiate the roles of immune checkpoints in autoimmunity versus autoinflammation.
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