| First Author | Montecino-Rodriguez EM | Year | 1991 |
| Journal | Immunology | Volume | 74 |
| Issue | 1 | Pages | 127-31 |
| PubMed ID | 1682243 | Mgi Jnum | J:2762 |
| Mgi Id | MGI:51284 | Citation | Montecino-Rodriguez EM, et al. (1991) Haematopoietic cell transfers between C57BL/6 mice differing at the lpr or gld locus. Immunology 74(1):127-31 |
| abstractText | The generalized lymphoproliferative disease (gld) and lymphoproliferation (lpr) mutations induce the development of strikingly similar autoimmune and lymphoproliferative syndromes in C57BL/6 mice (B6). These syndromes are characterized by hyperglobulinaemia, high levels of circulating autoantibodies and significant splenomegaly and lymphadenopathy resulting principally from the accumulation of a double negative CD4/CD8 T-cell population. These similarities led to the suggestion that the gld and lpr mutations affect two different steps of a common metabolic pathway controlling the differentiation of the T cells. By transferring haematopoietic cells into sublethally irradiated recipients we provide evidence for the different aetiology of the gld- and lpr-induced syndromes. The [gld----gld] chimaeras developed a gld-induced syndrome, like the [lpr----lpr] chimaeras developed a lpr-induced syndrome. However, in contrast to the severe lymphoid aplasia observed in the [lpr----wild] chimaeras, the [gld----wild] chimaeras showed an attenuated form of the gld-induced syndrome. The [lpr----gld] chimaeras developed a lymphoid aplasia (as in the [lpr----wild] chimaeras). This result shows that the gld environment cannot substitute for the lpr environment and allow for the emergence of an lpr-induced pathology. |
