| First Author | Huang D | Year | 2001 |
| Journal | Eur J Immunol | Volume | 31 |
| Issue | 1 | Pages | 225-32 |
| PubMed ID | 11265638 | Mgi Jnum | J:67001 |
| Mgi Id | MGI:1929589 | Doi | 10.1002/1521-4141(200101)31:1<225::AID-IMMU225>3.0.CO;2-0 |
| Citation | Huang D, et al. (2001) Disruption of the IL-1beta gene diminishes acetylcholine receptor-induced immune responses in a murine model of myasthenia gravis. Eur J Immunol 31(1):225-32 |
| abstractText | Human autoimmune myasthenia gravis (MG) is associated with the IL-1beta TaqI RFLP allele 2. Individuals positive for this allele have high levels of inducible IL-1beta in their peripheral blood. Here, we have characterized MG induction and the immune response elicited by Torpedo acetylcholine receptor (AChR) immunization in wild-type and IL-1beta deficient (-/-) mice. Compared with wild-type mice, IL-1beta-/- mice were relatively resistant to induction of clinical experimental autoimmune myasthenia gravis (EAMG). Draining lymph node cells from IL-1beta-/- mice showed poor proliferative capacity upon AChR stimulation in vitro. Both Th1 (IFN-gamma, IL-2) and Th2 (IL-4) cytokine responses were reduced and levels of serum anti-AChR antibodies decreased in IL-1beta-/- mice compared to wild-type mice. Taken together, these results reveal a critical role for IL-1beta in the induction of MG in mice, and support a role for IL-1beta in the pathogenesis of MG in man. |
