| First Author | Dittel BN | Year | 2000 |
| Journal | J Autoimmun | Volume | 14 |
| Issue | 4 | Pages | 311-8 |
| PubMed ID | 10882057 | Mgi Jnum | J:62703 |
| Mgi Id | MGI:1859473 | Doi | 10.1006/jaut.2000.0371 |
| Citation | Dittel BN, et al. (2000) Relapsing and remitting experimental autoimmune encephalomyelitis in B cell deficient mice. J Autoimmun 14(4):311-8 |
| abstractText | Experimental autoimmune encephalomyelitis (EAE) is an animal model for the human autoimmune central nervous system (CNS) disease multiple sclerosis (MS). To examine the role of B cells in EAE with a relapsing and remitting disease course (R-EAE) we generated (B10.PL x SJL/J)F1 mice deficient in B cells by disrupting their mu heavy chain transmembrane region (B10.PL x SJL/J)F1 muMT-/-. By immunizing (B10.PL x SJL/J)F1 and (B10.PL x SJL/J)F1 muMT-/- mice with the encephalitogenic N-terminal peptide Acl-11 of myelin basic protein (MBP), we observed that B-cell deficient mice exhibited a relapsing and remitting disease course. Since a similar day of onset and day of first relapse were observed these data suggest that B cells do not play a vital role in the activation of T cells leading to the initiation of EAE, nor in the reactivation of T cells resulting in R-EAE. |
