A novel alloreactivity-controlling locus, Alan1, mapped to mouse chromosome 17

The strength of the allotransplantation reaction depends on the genetic disparity between donor and recipient and on the genotype of the recipient. It has been shown that some inbred strains respond to alloantigens with a considerably stronger immune response than the other strains (Stepkowski and I...

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Bibliographic Details
Published in:Immunogenetics (New York) 2000-07, Vol.51 (8-9), p.755-757
Main Authors: Holán, V, Havelková, H, Krulová, M, Demant, P, Lipoldová, M
Format: Article
Language:English
Subjects:
Alan1 gene
allotransplantation
Animals
chromosome 17
Chromosome Mapping
Female
Isoantigens - immunology
Lymphocyte Culture Test, Mixed
Male
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Microsatellite Repeats
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Summary:The strength of the allotransplantation reaction depends on the genetic disparity between donor and recipient and on the genotype of the recipient. It has been shown that some inbred strains respond to alloantigens with a considerably stronger immune response than the other strains (Stepkowski and Ito 1990; Stewart et al. 1985). We have described previously that the proliferative response to alloantigens in MLC is controlled by a set of nonlinked genes which regulate the response irrespectively of the major histocompatibility complex (MHC)_genotype of stimulating cells (Holan et al. 1996). Since the proliferative response in MLC correlates with the survival of subsequent allografts as well as with graft-versus-host reaction (Bach 1970; Haeyry et al. 1972), the definition of genes controlling MLC responsiveness may improve the prediction of the transplantation outcome. To identify these genes, we are using a system of recombinant congenic strains (RCS) of mice produced and characterized by Demant and coworkers (Demant and Hart 1986; Stassen et al. 1996). In the RCS used in our experiments, random sets of approximately 12.5% genes from STS/A (STS) strain were transferred to the genetic background of BALB/cHeA (BALB/c) strain and a panel of 20 homozygous RCS of BALB/c-c-STS/Dem (CcS/Dem) series was prepared. The positions of STS segments in individual RCS were characterized by means of more than 600 microsatellite markers (Stassen et al. 1996). Using this approach we report here the identification of a novel alloreactivity-controlling locus, which we designate Alan1 (Alloantigen response 1) and which we mapped to mouse Chromosome (Chr) 17.
ISSN:0093-7711
1432-1211
DOI:10.1007/s002510000197