| First Author | Singh RR | Year | 2003 |
| Journal | J Immunol | Volume | 170 |
| Issue | 9 | Pages | 4818-25 |
| PubMed ID | 12707364 | Mgi Jnum | J:123824 |
| Mgi Id | MGI:3719734 | Doi | 10.4049/jimmunol.170.9.4818 |
| Citation | Singh RR, et al. (2003) Differential contribution of IL-4 and STAT6 vs STAT4 to the development of lupus nephritis. J Immunol 170(9):4818-25 |
| abstractText | Mechanisms that initiate lupus nephritis and cause progression to end-stage renal disease remain poorly understood. In this study, we show that lupus-prone New Zealand Mixed 2410 mice that develop a severe glomerulosclerosis and rapidly progressive renal disease overexpress IL-4 in vivo. In these mice, STAT6 deficiency or anti-IL-4 Ab treatment decreases type 2 cytokine responses and ameliorates kidney disease, particularly glomerulosclerosis, despite the presence of high levels of IgG anti-dsDNA Abs. STAT4 deficiency, however, decreases type 1 and increases type 2 cytokine responses, and accelerates nephritis, in the absence of high levels of IgG anti-dsDNA Abs. Thus, STAT6 and IL-4 may selectively contribute to the development of glomerulosclerosis, whereas STAT4 may play a role in autoantibody production. |
