| First Author | Yamagiwa S | Year | 1996 |
| Journal | Eur J Immunol | Volume | 26 |
| Issue | 7 | Pages | 1409-16 |
| PubMed ID | 8766540 | Mgi Jnum | J:34166 |
| Mgi Id | MGI:81635 | Doi | 10.1002/eji.1830260702 |
| Citation | Yamagiwa S, et al. (1996) Existence of a small population of IL-2R beta hi TCRint cells in SCG and MRL-lpr/lpr mice which produce normal Fas mRNA and Fas molecules from the lpr gene. Eur J Immunol 26(7):1409-16 |
| abstractText | Mice carrying the lpr gene, SCG and MRL-lpr/lpr mice, were used to characterize the phenotype and lpr gene of abnormally proliferating T cells in these mice. A major population which expanded in these mice were T cells expressing intermediate (int) levels of T cell receptor (TCR) (and CD3) and the phenotype of interleukin-2 receptor (IL-2R)beta(lo) alpha(-) (possibly abnormal TCR(int) cells). The levels of TCR(hi) cells of thymic origin (generated through the mainstream of T cell differentiation in the thymus) profoundly decreased after the onset of disease. However, a small population of normal TCR(int) cells (i.e. IL-2R beta(hi) alpha(-)) were also found to exist in all tested organs. For example, the majority of abnormal IL-2R beta(lo) TCR(int) cells were CD4(-)8(-) CD2(-), while normal IL-2R beta(hi) TCR(int) cells were a mixture of single-positive cells (mainly CD8(+)), CD4(-)8(-) cells and CD2(+) cells. Moreover, normal TCR(int) cells preferentially produced normal Fas mRNA and Fas molecules from the lpr gene. This phenomenon explains the leaky appearance of normal Fas mRNA and Fas molecules in mice carrying the lpr gene. It is suggested that a small population of IL-2R beta(hi) TCR(int) cells are resistant to the lpr genetic abnormality. |
