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Splenic lymphocytes from both the Storrs and Davis strains of muscular dystrophic chickens and the C57BL/6J-2J strain of muscular dystrophic mice cap FITC-Con A and FITC-Ig in a manner similar to normal controls. In analyses of testcross progeny of Storrs muscular dystrophic chickens, no difference in the ability of lymphocytes to cap were observed among the segregating progeny. Neither were any significant differences observed in lymphocyte capping among F2 segregating progeny of C57BL/6J-2J mice. These studies do not support the systemic membrane defect hypothesis for muscular dystrophy.

Hereditary muscular dystrophic chickens of the Storrs strain possess two genetic disorders, muscular dystrophy (MD) and a deficient concanavalin A (Con A), a T-cell mitogen, mediated splenic lymphocyte blastogenic response. A possible amelioration of the MD phenotype in MD chickens expressing normal Con A was postulated on the basis of progeny segregating for these two traits in F2 genetic analyses. To test this possibility, testcross progeny were examined for segregation of MD and Con A deficiency traits, and for the degree of muscle destruction and Con A deficiency. The data show both traits to be inherited independently as autosomal recessive traits, and do not support any phenotypic modifications occurring in chickens expressing MD with normal Con A. In the testcross progeny, the Con A deficiency disorder is equally deficient in normal and MD progeny, and the degree of muscle destruction as measured by serum creatine phosphokinase levels is equally great in MD chickens with or without the Con A deficiency trait. The reduced numbers of MD chickens in the testcross progeny can be accounted for by chance and probably reflect losses during in ovo development.

The Storrs strain of muscular dystrophic chickens were typed for erythrocyte alloalleles at 10 loci, including the B locus. Gene fixation is present at five loci and expression of the predominate alloantigen varied in frequency from 0.53 to 0.91 at the other five loci tested. The Storrs strain of muscular dystrophic chickens are not fixed at the B locus, expressing the B2/B2 allelic combination 81 percent of the time and B2/B23 the remaining percentage. Testcross progeny segregating for the muscular dystrophy trait did not show any alloantigen associations at the 10 loci examined. No association of the MD train with a particular B genotype could be ascertained. CPK levels as a measure of muscle destruction in the muscular dystrophic testcross progeny segregating at the B locus did not reveal an association with any B haplotype. Serum IgG levels and low Con A response in muscular dystrophic testcross progeny also were not associated with any specific B locus alloantigen combinations. The possibility remains that the establishment of a pathological index for muscular dystrophy in MD chickens may reveal an association with the B locus.

Plasma immunoglobulin profiles of New Hampshire strain muscular dystrophic chickens were determined by radial immunodiffusion, immunoelectrophoresis and polyacrylamide gel electrophoresis. Muscular dystrophic chickens have reduced levels of IgG but maintain normal levels of total serum proteins, IgA and IgM. The relationship and significance of the IgG deficiency to muscular dystrophy remains to be determined.