ABSTRACT
The mice were determined to lack both T and B cells, resulting in a disease similar to severe combined immunodeficiency as reported in humans. Homozygotes (scid/scid) maintained in barriers on sterilized food and water have no other gross lesions. Recently, Schwartz et al. described five human patients with impaired rearrangement processes at the JH region analogous to the defect in scid/scid mice. Nonobese diabetic mice spontaneously develop T-lymphocyte-mediated autoimmune insulitis and diabetes mellitus (type 1). Successful reports of transplantation of human neoplasms and xenogeneic hybridoma cells has led to the extensive use of scid/scid mice as hosts for normal and malignant tissue transplants. The scid mouse can serve as a bone marrow recipient to test this hypothesis by observing recipients of the bone marrow for development of the skin disease. The role of various aspects of the immune system on the pathogenesis of mouse mutations can be assessed by intercrossing the mutation being studied with the scid mutation.
