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Immunoregulatory changes in Kawasaki disease
1Division of HIV, Sexually Transmitted Diseases, Tuberculosis Laboratory Research,National Center for Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, 30333, USA.
Insights
Kawasaki disease (KD) involves immune system changes, particularly in T-lymphocytes. Treatment with intravenous gamma globulin (IVIG) alters these immune cell markers, suggesting T-cell involvement in KD vasculitis and potential elimination post-treatment.
Area of Science:
- Immunology
- Pediatric Rheumatology
- Vascular Biology
Background:
- Kawasaki disease (KD) is an acute vasculitis affecting young children.
- The etiology of KD remains unknown.
- Intravenous gamma globulin (IVIG) is the standard treatment to prevent cardiac complications.
Purpose of the Study:
- To investigate immune system alterations in KD patients before and after IVIG therapy.
- To examine T-lymphocyte activation, memory, and adhesion markers.
- To compare immune profiles between KD patients and healthy controls.
Main Methods:
- Three-color flow cytometry was used to analyze immune cell populations.
- KD patients were studied pre-IVIG, post-IVIG, and >40 days post-therapy.
- Comparison was made with age-matched pediatric controls and parents.
Main Results:
- Significant decreases in CD19, CD25, CD38, and CD71 positive cells were observed during convalescence compared to pre-IVIG.
- The proportion of CD3(+) T-lymphocytes increased post-treatment.
- Immune marker variability was highest in the patient with cardiac abnormalities.
Conclusions:
- T-lymphocytes play a role in the acute vasculitic process of KD.
- These findings suggest T-lymphocytes involved in endothelial damage are potentially cleared from peripheral blood after IVIG therapy.
- Immune dynamics in KD are complex and warrant further investigation.
Abstract:
Kawasaki disease (KD) is an acute vasculitis of unknown etiology, occurring in young children and treated with intravenous gamma globulin (IVIG) to prevent significant cardiac morbidity and mortality. We studied KD patients pre- and post-IVIG therapy and at >40 days posttherapy, additionally comparing them with matched pediatric control patients and parents. Using three-color flow cytometry, we examined immune changes in KD, especially previously unassessed markers of T-lymphocyte activation, memory, and adhesion. The percentage of cells positive for CD19, CD25, CD38, and CD71 was significantly lower during convalescence compared with pre-IVIG (medians: CD19, 18% vs 26%, P = 0.0004; CD25, 6% vs 9% for CD3(+) cells, P = 0.0074; CD38, 78% vs 89% for CD8(+) cells, P = 0.0015; CD71, 1% vs 6% for CD4(+) cells, P = 0.0024). The proportion of CD3(+) cells increased (medians: CD3, 66% vs 45%, P < 0.0001). Values for all parameters varied greatly pre- and post-IVIG, but not in a consistent direction. The sole patient with cardiac abnormalities had the greatest pre-/post-IVIG variability. These changes support the involvement of T-lymphocytes in the acute KD vasculitic process. They also suggest that T-lymphocytes involved in endothelial damage during acute KD may be subsequently removed or eliminated from the peripheral blood.