| First Author | Du C | Year | 2002 |
| Journal | J Immunol | Volume | 168 |
| Issue | 6 | Pages | 3105-12 |
| PubMed ID | 11884485 | Mgi Jnum | J:75323 |
| Mgi Id | MGI:2176322 | Doi | 10.4049/jimmunol.168.6.3105 |
| Citation | Du C, et al. (2002) Increased Severity of Experimental Allergic Encephalomyelitis in lyn(-/-) Mice in the Absence of Elevated Proinflammatory Cytokine Response in the Central Nervous System. J Immunol 168(6):3105-12 |
| abstractText | lyn, a member of the src kinase family, is an important signaling molecule in B cells. lyn(-/-) mice display hyperactive B-1 cells and IgM hyperglobulinemia. The role of lyn on T cell function and development of Th1-mediated inflammatory disease is not known. Therefore, we examined the effect of disruption of the lyn gene on the development of experimental allergic encephalomyelitis (EAE), a well-established Th1-mediated autoimmune disease. Following immunization with myelin oligodendrocyte protein (MOG) p35-55, lyn(-/-) mice had higher clinical and pathological severity scores of EAE when compared with wild type (WT). The increase in the severity of EAE in lyn(-/-) mice was not associated with a commensurate increase in the production of proinflammatory cytokines in the CNS. lyn(-/-) mice with EAE showed elevation in serum anti-IgM MOG Ab levels over that seen in WT mice, along with a modest increase in the mRNA levels of complement C5 and its receptor, C5aR, in the spinal cord. Transfer of serum from MOG-immunized lyn(-/-) mice worsened EAE in WT mice, suggesting a pathogenic role for anti-MOG IgM Abs in EAE. These observations underscore the potential role of lyn in regulation of Th1-mediated disease and the role of autoantibodies and complement in the development of EAE. |
