Naturally acquired anti‐αGal antibodies in a murine allograft model similar to delayed xenograft rejection.

Autor: Salvaris, Evelyn, Gock, Hilton, Han, Wenruo, Murray‐segal, Lisa, Barlow, Helen, Mottram, Patricia, Pearse, Martin, Cowan, Peter, Goodman, David, d’Apice, Anthony J. F.
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Zdroj: Xenotransplantation; Feb2000, Vol. 7 Issue 1, p42-47, 6p
Abstrakt: Abstract: Antibodies directed against galactose‐α1,3‐galactose (αGal) are believed to play an important a role in the pathogenesis of delayed xenograft rejection (DXR). This study was designed to determine whether α1,3‐galactosyltransferase‐deficient (Gal KO) mice can naturally acquire a sufficient anti‐αGal titre to cause the delayed type rejection of αGal‐expressing hearts. Gal KO mice of various ages were assessed for anti‐αGal antibody levels. αGal‐expressing hearts were transplanted heterotopically into these mice and monitored daily. Rejecting and surviving hearts were evaluated histologically. Results: in Gal KO mice greater than 6‐month‐old, 64% had an anti‐αGal antibody titre above the background level. When wild‐type αGal‐expressing hearts were transplanted into this group, 45% of grafts rejected within 5 to 13 days. Histological examination of the rejected hearts displayed marked tissue damage and an inflammatory infiltrate of predominantly macrophage/monocytes. Surviving grafts showed preserved morphology. Like humans, Gal KO mice naturally develop anti‐αGal antibodies with age. The titre in these mice was sufficient to cause a “delayed‐type” rejection of a significant proportion of αGal‐expressing cardiac grafts. This model thus provides an opportunity to investigate the role of naturally acquired anti‐αGal antibodies in the pathogenesis of DXR. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index