Control of inflammatory damage by anti-LFA-1: increase success of myoblast transplantation.
Myoblast transplantation is a potential treatment for Duchenne Muscular Dystrophy. This article confirms by experiments in mice that one problem that has limited the success of clinical trials of this procedure is a rapid (within 3 days) inflammatory reaction which kills most of the injected myoblasts. The death of the transplanted myoblasts can be prevented by treating the host with a mAb against LFA-1. This led to a 27-fold increase in the number of muscle fibers expressing a reporter gene present in the donor myoblasts when the host is also adequately immunosuppressed with FK506. Therefore, both the nonspecific inflammatory reaction and the specific immune response should be adequately controlled following myoblast transplantation.
Guérette
B
B
Centre de recherche en Neurobiologie, Université Laval, Québec, Canada.
Asselin
I
I
Skuk
D
D
Entman
M
M
Tremblay
J P
JP
D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001201:Ascites; D017690:Cell Transplantation; D003433:Crosses, Genetic; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D017930:Genes, Reporter; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007249:Inflammation / Q000517:prevention & control; D016169:Lymphocyte Function-Associated Antigen-1 / Q000276:immunology / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D008822:Mice, Transgenic; D018482:Muscle, Skeletal / Q000166:cytology*; D051381:Rats; D016559:Tacrolimus / Q000627:therapeutic use; D014184:Transplantation, Homologous / Q000276:immunology* / Q000473:pathology; D001616:beta-Galactosidase / Q000096:biosynthesis / Q000235:genetics
D000911:Antibodies, Monoclonal; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D016169:Lymphocyte Function-Associated Antigen-1; D001616:beta-Galactosidase; D016559:Tacrolimus