| First Author | Senju S | Year | 1996 |
| Journal | Int Immunol | Volume | 8 |
| Issue | 3 | Pages | 423-31 |
| PubMed ID | 8671629 | Mgi Jnum | J:31847 |
| Mgi Id | MGI:79350 | Doi | 10.1093/intimm/8.3.423 |
| Citation | Senju S, et al. (1996) Functional significance of the Fas molecule in naive lymphocytes. Int Immunol 8(3):423-31 |
| abstractText | The Fas molecule mediates apoptotic signal in many cell types. Mouse mutations (lpr, lprcg, gld), which impair the function of Fas, cause spontaneous autoimmune disease. We generated Fas-deficient (Fas-/-) mice by homologous recombination. In embryonic stem cells Fas-/- mice developed lpr-like disease, confirming that the abnormality of Fas is causal in the lpr phenotype. We also made Fas-/- chimeric mice composed of a mixture of Fas+/+ and Fas-/- cells. The chimeric mice also showed the lpr phenotype. In Fas-/-, chimeric mice, the Fas-deficient population expanded progressively among mature T and B lymphocytes. The expansion of Fas-deficient lymphocytes occurred at the naive, pre-primed, lymphocyte stage. These results suggest that the Fas molecule functions not only after antigenic stimulation, as previously hypothesized, but also at the naive lymphocyte stage. |
