| First Author | Singh AK | Year | 1994 |
| Journal | Immunol Invest | Volume | 23 |
| Issue | 4-5 | Pages | 281-92 |
| PubMed ID | 7959962 | Mgi Jnum | J:20382 |
| Mgi Id | MGI:68476 | Doi | 10.3109/08820139409066824 |
| Citation | Singh AK, et al. (1994) Interleukin-1 contributes to high level IgG production in the murine MRL/lpr lupus model. Immunol Invest 23(4-5):281-92 |
| abstractText | The autoimmune syndrome in MRL/lpr mice resembles human lupus, both in its serologic and immunopathologic characteristics. The contribution of IL-1 to high-level Ig production in the MRL/lpr model is poorly understood. We investigated the effect of treating B-cell-enriched, or, B plus T cell suspensions derived from either pre-disease or diseased lupus-prone MRL/lpr mice with IL-1 beta or IL-1 receptor antagonist (IL-1Ra). Disparate patterns of IgG production by B cells and B plus T cells derived from diseased versus pre-diseased MRL/lpr mice was observed following treatment with IL-1 beta. Remarkably, IL-1 beta caused significant suppression in IgG production by B cells derived from diseased MRL/lpr mice as compared to B cells derived from pre-disease mice. In mix-and-match experiments with B plus T cells from pre-disease and diseased MRL/lpr mice, both T cell help and B cell hyperactivity, originating in diseased MRL/lpr mice were found to be important factors in high-level IgG production in diseased MRL/lpr mice. Furthermore, IL-1Ra treatment of B plus T cell co-cultures derived from diseased MRL/lpr mice was able to significantly suppress IgG production, whereas, IL-1Ra treatment of B plus T cell co-cultures derived from pre-disease MRL/lpr mice demonstrated virtually no suppression in IgG production. Collectively, these results indicate a potentially important but complex role for IL-1 in influencing high-level IgG production in MRL/lpr mice with established disease. |
