| First Author | Bradshaw S | Year | 2008 |
| Journal | Clin Immunol | Volume | 129 |
| Issue | 1 | Pages | 19-30 |
| PubMed ID | 18692443 | Mgi Jnum | J:140403 |
| Mgi Id | MGI:3813747 | Doi | 10.1016/j.clim.2008.05.010 |
| Citation | Bradshaw S, et al. (2008) A role for Fli-1 in B cell proliferation: implications for SLE pathogenesis. Clin Immunol 129(1):19-30 |
| abstractText | Transgenic overexpression of Fli-1 in normal mice leads to SLE-like disease and increased expression was reported in SLE-affected human and murine lymphocytes. Reducing Fli-1 expression in MRL/lpr mice decreased antibody production, proteinuria, renal pathology, and mortality. Compared to those with wild-type expression of Fli-1, we report here that proliferative responses of Fli-1-deficient naive B cells to several mitogens were reduced in lupus-prone and control mice. Expression of mitogen receptors, including BCR, TLR4, and TLR9, was not significantly impacted in Fli-1-deficient naive B cells. IL12a transcripts were upregulated and NFAT transcripts were downregulated in Fli-1-deficient MRL/lpr B cells. These results demonstrate that Fli-1 deficiency affects B cell proliferative responses to mitogens, independent of BCR and TLR expression. IL12a and NFAT, known to influence proliferation, were identified as potential mediators of this effect. This may be a mechanism by which overexpression of Fli-1 contributes to B cell hyperactivity and subsequent SLE pathogenesis. |
