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Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
Published on: June 26, 2018
[Changes in CD69, CD25 and HLA-DR expressions in peripheral blood T cells in Kawasaki disease]
Yi-ying Zhang1, Xian-mei Huang, Man-li Kang
1Department of Cardiology, Children's Hospital Affiliated to Medical College, Zhejiang University, Hangzhou 310003, China.
Insights
Kawasaki disease (KD) involves increased T cell activation markers like CD69, CD25, and HLA-DR in patients. Intravenous immunoglobulin treatment reduced these markers, suggesting T cell activation contributes to cardiovascular injury in KD.
Area of Science:
- Immunology
- Pediatrics
- Cardiovascular Research
Context:
- Kawasaki disease (KD) is an acute febrile illness affecting young children.
- Cardiovascular complications, including coronary artery aneurysms, are a major concern in KD.
- T cell activation is implicated in the inflammatory processes of KD.
Purpose:
- To investigate the expression of T cell activation markers (CD69, CD25, HLA-DR) in peripheral blood T cells of children with KD.
- To assess the impact of intravenous immunoglobulin (IVIG) treatment on these T cell activation markers.
- To explore the relationship between T cell activation and cardiovascular injury in KD.
Summary:
- Flow cytometry revealed significantly higher percentages of CD69, CD25, and HLA-DR on T cells in acute KD patients compared to healthy controls.
- Following IVIG treatment, a significant decrease in CD69 and CD25 expression on T cells was observed, although the overall percentage of CD3+ T lymphocytes increased.
- No significant difference in T cell activation markers was found between KD patients with and without coronary artery abnormalities.
Impact:
- These findings highlight the role of T cell activation in the pathogenesis of Kawasaki disease.
- The study suggests that T cell activation may contribute to cardiovascular injury in KD patients.
- Monitoring T cell activation markers could offer insights into disease mechanisms and treatment response.
Objective:
The study was designed to investigate the changes in CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell in Kawasaki disease (KD).
Methods:
The authors detected CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell by using flow cytometry. The patients who met the diagnostic criteria for KD comprised sixteen boys and fifteen girls (4 - 60 months of age; mean, 26 +/- 18 months). All received intravenous gammaglobulin at a dose of 1 g/(kg.d), for 2 days and oral aspirin at a dose of 30 - 50 mg/(kg.d). In case of persistent fever, a repeated dose of intravenous gammaglobulin or I.V. methylprednisolone at a dose of 20 mg/(kg.d) for three daily doses was attempted. The authors tested blood samples from 17 healthy controls consisting of nine boys and eight girls (3 - 84 months of age; mean, 25 +/- 18 months) and the samples from 31 patients.
Results:
The percentage of peripheral blood CD(3)(+) T lymphocyte was (54.4 +/- 9.0)% in acute stage of KD and (65.0 +/- 7.0)% in healthy controls. There was a significant difference between the two groups (P < 0.001). The values of CD(69)(+) [(11.2 +/- 12.6)%, vs. (0.6 +/- 0.4)%], CD(25)(+) [(9.2 +/- 3.5)% vs. (3.9 +/- 1.8)%] and HLA-DR(+) [(8.3 +/- 5.0)% vs. (4.3 +/- 2.3)%] in KD patients were markedly increased compared to those of the healthy controls. After intravenous gammaglobulin treatment, the percentage of CD(3)(+)CD(69)(+) and CD(3)(+)CD(25)(+) significantly decreased [CD(3)(+)CD(69)(+): (14.0 +/- 13.0)% vs. (1.6 +/- 1.2)%, P < 0.05; CD(3)(+)CD(25)(+): (7.8 +/- 4.1)% vs. (2.0 +/- 0.6)%, P < 0.01]. However, the CD(3)(+) T lymphocytes increased [(50.8 +/- 5.0)% vs. (64.9 +/- 5.5)%, P < 0.01]. There was no significant difference in expression of CD(3)(+) T lymphocyte cell activating markers between coronary artery disease group and normal coronary artery group in KD cases (P > 0.05).
Conclusion:
CD(3)(+) T cell activation in the early and middle stages is involved in the mechanism responsible for cardiovascular injury.