In:
The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 93.8-93.8
Abstract:
The pathogenesis of Kawasaki disease (KD) is not clear, but certain genetic defects of inhibitory immune processes after infectious stimuli have been suspected as a feasible factor. In the present study, we investigated the associative roles of programmed death-1 (PD-1) gene in the pathogenesis of KD. In order to induce KD-like manifestations in young PD-1KO mice, injection of the bacilli Calmette Guérin (BCG) was performed twice with a 4 week interval. After the second injection, PD-1KO mice showed KD-like clinical features including prolonged fever for more than 5 days, erythematous swelling on soles, anal desquamation, and gallbladder (GB) hydrops. Inflammation in at least more than one coronary artery was found in all PD-1KO mice whereas scanty coronary lesion was found in wild type (WT) mice. When the PD-1KO mice were challenged twice with HSP65 as same methods of BCG, coronary arterial lesions similar to those seen after BCG injection were observed. Inflammatory reactions in other organs including hepatic arteries, renal arteries, and biliary arteries were observed in PD-1KO mice. The levels of Interferon-γ and IL-6 were significantly increased in both sera and splenocytes of PD-1KO mice compared with WT mice (P & lt; 0.05). These results suggest that KD may develop in genetically prone populations by microorganism containing HSP65, and PD-1 gene may be an important component among genetic predispositions of KD.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.184.Supp.93.8
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2010
detail.hit.zdb_id:
1475085-5
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