Premium
Effect of intravenous immunoglobulin on inhibiting peripheral blood lymphocyte apoptosis in acute Kawasaki disease
Author(s) -
Yi QJ,
Li CR,
Yang XQ
Publication year - 2001
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.2001.tb02423.x
Subject(s) - medicine , apoptosis , aspirin , dna fragmentation , lymphocyte , immunology , antibody , pathogenesis , monoclonal antibody , peripheral blood lymphocyte , kawasaki disease , monoclonal , programmed cell death , biology , biochemistry , artery
This study aimed to explore the therapeutic mechanism of intravenous immunoglobulin (IVIG) for Kawasaki disease (KD) Peripheral blood lymphocytes (PBLs) obtained from 26 children with KD and 20 age‐matched healthy children were stimulated with anti‐CD 3 monoclonal antibody (mAb), and the percentage of apoptotic cells and DNA fragmentation were assayed at 0, 12, 24, 48 and 72 h in vitro. The patients were divided into two groups: one treated with aspirin combined with IVIG ( n = 16) and one treated with aspirin alone ( n = 10). PBLs were stimulated by phytohaemag‐glutinin to evaluate the lymphocyte proliferative response. Compared with normal controls, the apoptotic cell percentage and the DNA fragmentation were markedly decreased ( p < 0.001) and delayed in PBLs from KD patients. After IVIG treatment, the decreased percentage of apoptotic cell and delayed DNA fragmentation were restored to the state of the normal controls, accompanied by a fast clinical remission compared with the aspirin‐alone group. The lymphocyte proliferative response was also decreased 3–5 d after IVIG therapy ( p < 0.001). Conclusion : The results suggest that decreased PBL apoptosis may be involved in the pathogenesis of KD. The therapeutic mechanism of IVIG in KD may be partially due to the reversal of the inhibited lymphocyte apoptosis, and may have implications for other autoimmune diseases with inefficient lymphocyte apoptosis.