Correction of gld autoimmunity by co-infusion of normal bone marrow suggests that gld is a mutation of the Fas ligand gene

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Abstract
lpr and gld mice develop phenotypically indistinguishable systemic autoimmune diseases and marked lymphadenopathy dominated by CD4−CD8−In vivo chimera experiments have demonstrated that both ipr T and ipr B cells are intrinsically defective. Analogous experiments were conducted using gld mice. Lethally irradiated gld mice were given mixtures of congenic gld and normal (+/+) bone marrow differentially marked by lg heavy chain allotype. In sharp contrast to ipr-+/+ mixed chimeras, gld-+/+ chimeras had little autoantibody production at 5 months and minimal adenopathy at 6 months, indicating that the normal marrow-derived cells corrected the gld defect. Thus, aberrant autoantibody production is due to a defect extrinsic to the gld B cell and lymphoproliferation is due to a defect extrinsic to the gld T cell. These data support the hypothesis that gld mice lack an apoptosis-inducing ligand. The receptor for this ligand may be the Fas molecule, which is defective in ipr mice T cells.

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