Inflammatory damage following first-generation replication-defective adenovirus controlled by anti-LFA-1

被引:7
作者
Guerette, B
Moisset, PA
Huard, C
Tardif, F
Gravel, C
Tremblay, JP
机构
[1] HOP ENFANTS JESUS,CTR RECH NEUROBIOL,QUEBEC CITY,PQ G1J 1Z4,CANADA
[2] UNIV LAVAL,CTR RECH NEUROBIOL,QUEBEC CITY,PQ,CANADA
[3] UNIV LAVAL,CTR RECH,LAB TRANSFERT GENES,BEAUPORT,PQ,CANADA
关键词
macrophage; neutrophil; respiratory burst; FK506; Duchenne muscular dystrophy;
D O I
10.1002/jlb.61.4.533
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
First-generation replication-defective adenoviruses have been reported to lead to transient reporter gene expression due to a specific immune reaction involving T and B lymphocytes. Some recent reports have also demonstrated the presence of a nonspecific inflammatory reaction involving macrophages and neutrophils after both intramuscular injections and viral vectors transduction. To further investigate this nonspecific inflammatory reaction, Delta E-1/E-3(a) adenoviruses were injected intramuscularly in immunocompetent mice. Some of these mice were treated with anti-LFA-1. The adenovirus-injected muscles showed abundant CD4(+), CD8(+), LFA-1(+), and Mac-1(+) cell infiltration 3 days after the Delta E-1/E-3(a) injection. The anti-LFA-1 monoclonal antibody was able to block the nonspecific inflammatory damage due mostly to neutrophils and macrophages. The anti-LFA-1 did not produce this effect by reducing the muscle infiltration by LFA-1(+) cells, It may instead have blocked the direct interaction between LFA-1 and ICAM-1 thus preventing the damage produced by the respiratory burst of neutrophils, Blocking the resulting damage of this inflammatory reaction with anti-LFA-1 in animals also treated with FK506, a powerful immunosuppressant for gene therapy, largely increased the long-term transgene expression compared with mice only treated with FK506.
引用
收藏
页码:533 / 538
页数:6
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