The Journal of Experimental Medicine
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The Journal of Experimental Medicine, Vol 129, 1013-1027, Copyright © 1969 by The Rockefeller University Press


ARTICLE

GENE CONTROL OF HEMATOPOIESIS : I. ERYTHROCYTE MOSAICISM AND PERMANENT IMMUNOLOGICAL TOLERANCE IN ALLOPHENIC MICE



Beatrice Mintz Ph.D.1 and Joy Palm Ph.D.1

1 From The Institute for Cancer Research, Fox Chase, Philadelphia, Pennsylvania 19111, and The Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104

Erythropoietic cells of two unrelated strains, C3H (or C3Hf) and C57BL/6, can coexist throughout hematopoiesis in allophenic mice experimentally produced from aggregated, undifferentiated blastomeres of separate genotypes. The presence of two red cell genotypes in these circumstances signifies that the erythroid population must normally be multiclonal, i.e., derived mitotically from at least two genetically determined cells. The two strains were detected by hemagglutination and absorption tests of erythrocytes for the specific histocompatibility antigens dictated by the H-2k and H-2b alleles.

Of 34 C3H(f) harr C57BL/6 allophenics tested, 16 had both red cell types; the remaining 18 showed only C3H or C57 red cells and included 12 mice with both cell strains present in some other tissues. All animals with evidence of two H-2 phenotypes among circulating erythrocytes were permanently immunologically tolerant of both antigenic types and remained free of runt disease. They lived a full lifespan, up to 2 yr 7frac12 months of age.

The data suggest a possible specific selective advantage of C57BL/6 over C3H erythropoietic tissue. There is considerable individual variability, not only in proportions of antigenically distinct erythrocytes, but also in strain composition of other tissues in the same animals. A broad spectrum of distinctive situations is found, in which parameters are varied within or outside of the circulatory system. Allophenic mice can therefore serve as investigative tools for entirely new kinds of experimental studies of gene control mechanisms and blood physiology in normal hematopoiesis and in a number of hereditary blood diseases.

Submitted on December 15, 1968


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