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GENETIC CONTROL OF PQ PROLONGATION OF THE ELECTROCARDIOGRAM IN THE MOUSE IMMUNIZED WITH THE KILLED GROUP A STREPTOCOCCI
Author(s) -
Matsunaga K.,
Tani K.,
Katoh K.,
Ishigatsubo Y.,
Iwaku T.,
Tadokoro,and I.,
Okuda K.
Publication year - 1983
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/j.1744-313x.1983.tb01014.x
Subject(s) - congenic , haplotype , prolongation , biology , major histocompatibility complex , gene , antibody , pathogenesis , histocompatibility , genetics , immune system , microbiology and biotechnology , immunology , antigen , allele , medicine , human leukocyte antigen
SUMMARY Genetic control of PQ prolongation of the electrocardiogram (ECG) in the mouse, immunized with killed group A streptococci, was studied by using various congenic mice. Mice of H‐2 a , H‐2 k and H‐2 f haplotypes showed high frequencies of PQ prolongation, while haplotypes of H‐2 b , H‐2 d and H‐2 s showed low frequencies of PQ prolongation. Studies using various recombinant mice revealed that at least one immune‐associated (Ir) gene mapped in the left side of the I‐B subregion. High responsiveness of F 1 hybrids of H‐2 b and H‐2 d , as well as B1O.A(5R) and B10.A(3R), suggests the existence of a complementing gene. In addition, the differences between C3H and CKB, as well as differences between C3H.SW and CWB, indicate that another Ir gene maps in the immunoglobulin heavy chain (Igh) coding loci. Repeated injections of anti‐ I‐J or anti‐ I‐A antisera also modified this PQ prolongation. These results suggested that both the major histocompatibility complex (MHC) and immunoglobulin (Igh) loci seem to be playing important roles in the pathogenesis of PQ prolongation.