| First Author | Parker Harp CR | Year | 2015 |
| Journal | J Immunol | Volume | 194 |
| Issue | 11 | Pages | 5077-84 |
| PubMed ID | 25895531 | Mgi Jnum | J:274832 |
| Mgi Id | MGI:6220514 | Doi | 10.4049/jimmunol.1402236 |
| Citation | Parker Harp CR, et al. (2015) B cell antigen presentation is sufficient to drive neuroinflammation in an animal model of multiple sclerosis. J Immunol 194(11):5077-84 |
| abstractText | B cells are increasingly regarded as integral to the pathogenesis of multiple sclerosis, in part as a result of the success of B cell-depletion therapy. Multiple B cell-dependent mechanisms contributing to inflammatory demyelination of the CNS have been explored using experimental autoimmune encephalomyelitis (EAE), a CD4 T cell-dependent animal model for multiple sclerosis. Although B cell Ag presentation was suggested to regulate CNS inflammation during EAE, direct evidence that B cells can independently support Ag-specific autoimmune responses by CD4 T cells in EAE is lacking. Using a newly developed murine model of in vivo conditional expression of MHC class II, we reported previously that encephalitogenic CD4 T cells are incapable of inducing EAE when B cells are the sole APC. In this study, we find that B cells cooperate with dendritic cells to enhance EAE severity resulting from myelin oligodendrocyte glycoprotein (MOG) immunization. Further, increasing the precursor frequency of MOG-specific B cells, but not the addition of soluble MOG-specific Ab, is sufficient to drive EAE in mice expressing MHCII by B cells alone. These data support a model in which expansion of Ag-specific B cells during CNS autoimmunity amplifies cognate interactions between B and CD4 T cells and have the capacity to independently drive neuroinflammation at later stages of disease. |
