Gene therapy to inhibit xenoantibody production using lentiviral vectors in non-human primates View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-01

AUTHORS

J Y Fischer-Lougheed, A F Tarantal, I Shulkin, N Mitsuhashi, D B Kohn, C C I Lee, M Kearns-Jonker

ABSTRACT

Xenoantibodies to the gal alpha1,3 gal (gal) epitope impede the use of pig tissues for xenotransplantation, a procedure that may help overcome the shortage of human organ donors. Stable gal chimerism and tolerance to gal(+) hearts could be achieved in alpha1,3-galactosyltransferase (alpha1,3GT)(-/-) mice using lentiviral vectors expressing porcine alpha1,3GT, the enzyme that synthesizes the gal carbohydrate. In this study, we evaluated whether chimerism sufficient to inhibit anti-gal xenoantibody responses can be achieved using lentivectors in non-human primates. Rhesus macaques were transplanted with autologous, alpha1,3GT-transduced bone marrow (BM) following sublethal irradation. Simian immunodeficiency virus (SIV)- and human immunodeficiency virus (HIV)-1-derived lentiviral constructs were compared. Chimerism was observed in several hematopoietic lineages in all monkeys. Engraftment in animals receiving SIV-based alpha1,3GT constructs was similar to that achieved using the HIV-1-derived lentivector for the first 2 months post-transplantation, but increased thereafter to reach higher levels by 5 months. Upon immunization with porcine hepatocytes, the production of anti-gal immunoglobulin M xenoantibody was substantially reduced in the gal(+) BM recipients compared to controls. This study is the first to report the application of gene therapy to achieve low-level, long-term gal chimerism sufficient to inhibit production of anti-gal antibodies after immunization with porcine cells in rhesus macaques. More... »

PAGES

49

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.gt.3302818

DOI

http://dx.doi.org/10.1038/sj.gt.3302818

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001592873

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16886002


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