| First Author | Segal BM | Year | 1996 |
| Journal | J Exp Med | Volume | 184 |
| Issue | 2 | Pages | 771-5 |
| PubMed ID | 8786337 | Mgi Jnum | J:35316 |
| Mgi Id | MGI:82766 | Doi | 10.1084/jem.184.2.771 |
| Citation | Segal BM, et al. (1996) IL-12 unmasks latent autoimmune disease in resistant mice. J Exp Med 184(2):771-5 |
| abstractText | Inbred mice exhibit a spectrum of susceptibility to induction of experimental allergic encephalomyelitis (EAE). We have compared the immune responses of the susceptible SJL (H-2s) and resistant B10.S (H-2s) strains to determine factors other than the MHC background which control resistance/susceptibility to EAE. The resistance of the B10.S strain was found to be secondary to an antigen-specific defect in the generation of Th 1 cells that produce IFN gamma. This defect in IFN gamma production could be restored by exposure of the myelin basic protein (MBP)-reactive T cells to IL-12 with the subsequent induction of the ability to transfer EAE to naive recipients. These findings have important implications for the therapeutic use of IL-12 and IL-12 antagonists and may explain the association between relapses/exacerbation of autoimmune disease and infectious diseases. |
