Premium
Presence of Human Chromosome 1 with Expression of Human Decay‐Accelerating Factor (DAF) Prevents Lysis of Mouse/Human Hybrid Cells by Human Complement
Author(s) -
WANG M.W.,
WRIGHT L. J.,
SIMS M. J.,
WHITE D. J. G.
Publication year - 1991
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1991.tb01602.x
Subject(s) - decay accelerating factor , biology , complement system , cd46 , monoclonal antibody , lysis , factor h , locus (genetics) , gene , microbiology and biotechnology , antibody , chromosome , complement (music) , complement factor i , genetics , phenotype , complementation
Xenogeneic organs transplanted to phylogenetically distant species are subject lo rapid destruction mediated by complement. In humans, the complement activation is regulated by several proteins encoded by a series of closely linked genes (RCA locus) located on chromosome I. The mouse/human hybrid cell line BIO was found to have retained human chromosome I, FACS analysis confirmed that RCA products such as decay‐accelerating factor (DAF) were expressed on the membrane surface of B10 cells. When exposed to human or rabbit complement in the presence of naturally occurring’human anti‐mouse antibodies these cells were not lysed by human complement but were killed by rabbit complement. This effect could be abrogated by addition of anti‐DAF monoclonal antibody (IC6). The results offer potential for genetic manipulation of the human complement regulatory products in animals lo overcome xenograft hyperacute rejection.