| First Author | Mayo S | Year | 2007 |
| Journal | Clin Immunol | Volume | 122 |
| Issue | 1 | Pages | 91-100 |
| PubMed ID | 16990050 | Mgi Jnum | J:116632 |
| Mgi Id | MGI:3694599 | Doi | 10.1016/j.clim.2006.08.001 |
| Citation | Mayo S, et al. (2007) Altered susceptibility to EAE in congenic NOD mice: Altered processing of the encephalitogenic MOG35-55 peptide by NOR/LtJ mice. Clin Immunol 122(1):91-100 |
| abstractText | NOD mice (H-2 g7) naturally develop autoimmune diabetes, while the congenic NOR/LtJ mice (H-2 g7) are resistant. To determine if defective immune regulation renders NOD susceptible to autoimmune disease, we compared MOG35-55-induced EAE in NOD mice to that of NOR/LtJ. In two of three immunization protocols, the NOR/LtJ mice developed significantly reduced indices and severity of clinical disease, in spite of an exaggerated autoimmune response to MOG35-55. Characterization of the responding T cell repertoires revealed that V beta 8+ Th cells directed toward the MOG42-55 core epitope were dominant in both strains. Interestingly, CD8+ CTL were absent or significantly reduced in MOG35-55 lymphoblasts from NOR/LtJ mice, which poorly processed the MOG39-47 CTL epitope from MOG35-55. Thus, while particular MHC class II alleles may be associated with increased risk, molecules involved in the processing of key epitopes may be influential in the progression of autoimmune disease. |
