FK506 Immunosuppression to Control the Immune Reactions Triggered by First-Generation Adenovirus-Mediated Gene Transfer

Vilquin, Jean‐Thomas; Guérette, B.; Kinoshita, Ikuo; Roy, Brigitte; Goulet, M; Gravel, Claude; Roy, Raynald; Tremblay, Jacques P.

doi:10.1089/hum.1995.6.11-1391

Cited by 153 publications

(81 citation statements)

References 56 publications

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“…FK506 did not induce long-term tolerance of the neo-antigen ␤-gal, but may slow the rejection reaction, as observed in other experimental situations. 37,41 Our results thus confirm that ␤-gal antigens may trigger immune reactions, even in the absence of a cellular or viral vector. 37 The present results were obtained in the C57BL6J mouse strain, using a transgene of prokaryotic origin.…”

Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutsupporting

confidence: 72%

“…37,41 Our results thus confirm that ␤-gal antigens may trigger immune reactions, even in the absence of a cellular or viral vector. 37 The present results were obtained in the C57BL6J mouse strain, using a transgene of prokaryotic origin. It should be underlined that the triggering and extent of immune rejection may vary according to the nature of the transgene product and the animal species or strain.…”

Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutsupporting

confidence: 72%

“…We did not observe the massive cellular infiltration that is present following delivery of cellular or viral vectors. 36,37 Given the fibrotic nature of the dystrophic muscles, it is difficult to judge about the potential damage triggered by electrotransfer in the models of muscular dystrophies.…”

Section: Resultsmentioning

confidence: 99%

“…[54][55][56][57][58] FK506 has been used previously to prevent the rejection of transgene products brought in recipient animals by cellular or viral vectors. [37][38][39][40][41][42][43][44] Our present results indicate that the specific immune reactions are blocked by the permanent or discontinuous administration of the FK506 immunosuppressant. The protection, however, fades away and the number of ␤-gal-positive fibers decreases with time after termination of FK506.…”

Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutmentioning

confidence: 88%

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Electrotransfer of naked DNA in the skeletal muscles of animal models of muscular dystrophies

Vilquin

Kennel²,

Paturneau-Jouas

et al. 2001

Gene Ther

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The electrotransfer of naked DNA has recently been adapted to the transduction of skeletal muscle fibers. We investigated the short-and long-term efficacy of this methodology in wild-type animals and in mouse models of congenital muscular dystrophy (dy/dy, dy 2J /dy 2J ), or Duchenne muscular dystrophy (mdx/mdx). Using a reporter construct, the short-term efficacy of fiber transduction reached 40% and was similar in wild-type, dy/dy and dy 2J /dy 2J animals, indicating that ongoing muscle fibrosis was not a major obstacle to the electrotransfer-mediated gene transfer. Although the complete rejection of transduced fibers was observed within 3 weeks in the absence of immunosuppression, the persistency was prolonged over 10 weeks when transient or continuous immunosuppressive regimens were used. Using

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Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutsupporting

confidence: 72%

Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutsupporting

confidence: 72%

Section: Resultsmentioning

confidence: 99%

Section: Figure 7 Lack Of Persistence Of Transduced Fibers In An Acutmentioning

confidence: 88%

See 2 more Smart Citations

Electrotransfer of naked DNA in the skeletal muscles of animal models of muscular dystrophies

Vilquin

Kennel²,

Paturneau-Jouas

et al. 2001

Gene Ther

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“…In fact, administration of immunosuppressive agents such as CTLA4Ig and FK506 has been shown to sustain transgene expression after adenovirus injection in skeletal muscle. 56,57 However, preliminary studies with HSV amplicons have yielded successful results with our treatments. The use of non-replicating, relatively non-toxic HSV amplicons with our proposed treatments could further alleviate the immunogenicity of foreign protein expression in skeletal muscle.…”

Section: Treatmentmentioning

confidence: 99%

Efficient infection of mature skeletal muscle with herpes simplex virus vectors by using dextran sulfate as a co-receptor

1999

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The use of herpes simplex virus (HSV) vectors for gene chondroitin ABC lyase, HSV infection was restored, which delivery to skeletal muscle is hampered by a maturationsuggests that virus secondary receptors were present but dependent loss of muscle fiber infectivity. Previous studies not readily accessible to the virus in the intact myofiber. of HSV type 1 (HSV-1) infection in the rodent show that Surprisingly, we also found that HSV-1 infectivity could be the loss of infectivity may be due, at least in part, to the restored in vitro and in vivo by exposing myofibers to low development of the basal lamina throughout the course of concentrations of the glycosaminoglycan analog dextran maturation, which may block the initial events in HSV infecsulfate, which appears to act as a surrogate receptor to tion. To initiate infection, HSV normally attaches to cell surstabilize the virus at the myofiber surface such that HSV face heparan sulfate, which stabilizes the virus such that can engage additional receptors. This demonstration that it can interact with secondary protein receptors required the basal lamina is not an absolute block to HSV-1 infecfor entry into host cells. In this study, we demonstrate that tion is remarkable because it allows for the nondestructive heparan sulfate biosynthesis is downregulated during skeltargeting of HSV-1 to mature myofibers and greatly etal muscle maturation. When myofibers were treated with expands the usefulness of HSV as a gene therapy vector a variety of enzymes, including collagenase type IV or for the treatment of inherited and acquired diseases.

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Progress in myoblast transplantation: a potential treatment of dystrophies

Skuk

Tremblay

2000

Microsc. Res. Tech.

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Myoblast transplantation (MT) consists of injecting normal or genetically modified myogenic cells into muscles, where they are expected to fuse and form mature fibers. As an experimental approach to treat severe genetic muscle diseases, MT was tested in dystrophic patients at the beginning of the 1990s. Although these early clinical trials were unsuccessful, MT has progressed through the research on animal models. Many factors that may condition the success of MT were identified in the last years. The present review updates our knowledge on MT and describes the different problems that have limited its success. Factors that were first underestimated, like the specific immune response after MT, are presently well characterized. Destruction of the hybrid fibers by activated T‐lymphocytes and production of antibodies against the transplanted myoblasts take place after MT and are responsible for the graft rejection. The choice of the immunosuppression seems to be very important, and FK506 is the best agent known to allow the best results after MT. Under FK506 immunosuppression, very efficient MT were obtained both in mice and monkeys. Moreover, in dystrophic mice it was demonstrated that MT ameliorates some phenotypical characteristics of the disease. The improvement of the survival of the transplanted cells and the increase of their migration into the injected tissue are presently under investigation. Some of the present research is directed also to bypass the immunosuppression by using the patient's own cells for MT. In this sense, efforts are conducted to introduce the normal gene into the patient's myoblasts before MT and to improve the ability of these cells to proliferate in vitro. Micros. Res. Tech. 48:213–222, 2000. © 2000 Wiley‐Liss, Inc.

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FK506 Immunosuppression to Control the Immune Reactions Triggered by First-Generation Adenovirus-Mediated Gene Transfer

Cited by 153 publications

References 56 publications

Electrotransfer of naked DNA in the skeletal muscles of animal models of muscular dystrophies

Electrotransfer of naked DNA in the skeletal muscles of animal models of muscular dystrophies

Efficient infection of mature skeletal muscle with herpes simplex virus vectors by using dextran sulfate as a co-receptor

Progress in myoblast transplantation: a potential treatment of dystrophies

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