| First Author | Sobel ES | Year | 1993 |
| Journal | Int Immunol | Volume | 5 |
| Issue | 10 | Pages | 1275-8 |
| PubMed ID | 7505611 | Mgi Jnum | J:22004 |
| Mgi Id | MGI:66426 | Doi | 10.1093/intimm/5.10.1275 |
| Citation | Sobel ES, et al. (1993) Correction of gld autoimmunity by co-infusion of normal bone marrow suggests that gld is a mutation of the Fas ligand gene. Int Immunol 5(10):1275-8 |
| abstractText | lpr and gld mice develop phenotypically indistinguishable systemic autoimmune diseases and marked lymphadenopathy dominated by CD4-CD8- T cells. In vivo chimera experiments have demonstrated that both lpr T and lpr 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 Ig heavy chain allotype. In sharp contrast to lpr-(+)/+ 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 lpr mice. |
