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From the Department of Microbiology, The Medical College of Wisconsin, Milwaukee, Wisconsin 53233
Abstract
The autosomal recessive pituitary Ames dwarf mouse was immunodeficient as shown by lymphocyte depletion and involution of thymus and peripheral lymphoid tissue, lymphopenia and a wasting syndrome with subsequent death at a young age. The appearance of 19S and 7S hemolytic plaque-forming cells after immunogenic stimulation with sheep erythrocytes was delayed and considerably less in Ames dwarf mice than in normal littermates. The graft-vs-host reactivity of spleen cells, measured by the Simonsen splenomegaly assay in young (Ames x AKR)F1 hybrid mice, was significantly lower in Ames dwarf mice. On the other hand, the Ames dwarf mouse did not have marked deficiencies in the serum levels of immunoglobulin. The normal colony-forming capacity of bone marrow cells measured with the spleencolony assay of Till and McCulloch (see Ref. 13), suggested a normal stem cell population in the bone marrow of Ames dwarf mice. The earliest degenerative change of the thymus of the Ames dwarf mouse was a depletion of thymocytes from the thymus cortex frequently accompanied by an increased number of lymphoid cells in the medulla. This was followed by a loss of lymphoid cellularity of the medulla, thereby causing a complete involution of the thymus. These results suggest that the Ames dwarf mouse has an immunodeficiency of the thymus-dependent lymphoid system as a consequence of defective thymotropic influences by the pituitary.
Footnotes
1 The study was supported by grants from the American Cancer Society (Minnesota and Milwaukee Divisions), the Minnesota Heart Association, The Research Corporation and PHS General Research Grant 5 SO1 FR-5434.
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