| First Author | Katsume A | Year | 1997 |
| Journal | Clin Immunol Immunopathol | Volume | 82 |
| Issue | 2 | Pages | 117-24 |
| PubMed ID | 9000479 | Mgi Jnum | J:38308 |
| Mgi Id | MGI:85684 | Doi | 10.1006/clin.1996.4278 |
| Citation | Katsume A, et al. (1997) Interleukin-6 overexpression cannot generate serious disorders in severe combined immunodeficiency mice. Clin Immunol Immunopathol 82(2):117-24 |
| abstractText | C57BL/6 human interleukin-6 (IL-6) transgenic mice develop mesangial proliferative glomerulonephritis with massive IgG1 plasmacytosis and die of renal failure in early life. To test whether the IL-6 overexpression could cause development of mesangial proliferative glomerulonephritis without plasmacytosis or promote proliferation of immature B cells that have not undergone immunoglobulin gene rearrangement, the IL-6 transgene was introduced into mice with severe combined immunodeficiency (SCID). In the immunocompetent littermate IL-6 transgenic mice, there were various symptoms such as plasmacytosis, nephropathy, anemia, and thrombocytosis, accompanied by marked increases in serum IL-6 levels as they aged. All these mice died by 25 weeks of age. In contrast, the SCID-IL-6 transgenic mice had no such abnormalities, except certain hematological changes, although the transgene was expressed in various tissues. In these mice, the serum IL-6 levels were 10- to 15-fold higher than those in the nontransgenic mice, and they remained constant throughout their lives. Furthermore, there were no signs of lymphoid development. This study demonstrates that deregulation of IL-6 expression does not stimulate cell growth or differentiation of immature B cells, and thus does not result in plasmacytosis and age-related increases in IL-6 production, and also does not generate mesangial proliferative glomerulonephritis. |
