Abstract
Short-lived SAMP-P/1 mice are low responders in in vitro antibody responses because of a selectively impaired helper T(Th)-cell activity. After crossing with high responders (B10.BR mice), about 12% of (B10.BR x SAM-P/1) (BRP)F2 mice showed low responsiveness, as did SAM-P/1 mice, against two T-dependent antigens, sheep and horse red blood cells (RBC), both of which were not cross-reactive to each other at helper T- and B-cell levels. The immune activities against the two antigens in individual BRPF2 mice showed a good correlation (r = 0.81), thereby suggesting that SAM-P/1 mice have an antigen non-specific Th cell dysfunction. Based on the incidence of the low responders in F2 generation and statistical analyses, the hypo-responsiveness was postulated to be controlled by two genes. To survey the location of these genes, linkage analyses were performed in the F2 mice using a large set of genetic markers. Low responders in the F2 generation showed a significantly higher incidence of SAM-P/1 genotype at the Gpi-1 as well as c locus on chromosome 7 (Chr.7). However, no linkage of low responsiveness to the Hbb locus was evident, an area present at a more distal site to the centromere on the same chromosome. These results suggest that one of the genes controlling the hypo-responsiveness of SAM-P/1 mice is linked to both Gpi-1 and c loci and that it locates at a more proximal site on Chr.7.
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