Myelination of mouse axons by Schwann cells transplanted from normal and abnormal human nerves

Abstract

IN mouse nerve iso- and allografts, Schwann cells transplanted from the donor animal survive, multiply within the graft and, eventually, ensheath axons regenerating from the host nerve^1–3. This demonstration of the persistence of donor cells in nerve grafts has made possible the in vivo study of cell interactions in genetically-determined animal neuropathies. By combining normal and abnormal nerves, each originating from different strains of mice, a primary Schwann cell abnormality has been demonstrated in Trembler³ and Quaking⁴ mutant mice while axonal factors seem to be responsible for changes in the spinal roots of dystrophic mice^5,6. We report here the successful transplantation into immunologically-suppressed mice of human Schwann cells from control patients and from the sural nerve of a child with metachromatic leukodystrophy. Metachromatic leukodystrophy (MLD) is a human autosomal recessive disease due to aryl sulphatase deficiency and characterised by degeneration in the central and peripheral nervous systems with intracellular accumulations of metachromatic granules^7,8.