Table 3.
The role of B cells in experimental autoimmune encephalomyelitis (EAE) animal models.
| Reference | Year | Findings |
|---|---|---|
| Hjelmstrom et al. (92) | 1998 | B cell-independent demyelination in myelin oligodendrocyte glycoprotein (MOG)-induced EAE mice |
| Litzenburger et al. (89) | 1998 | MOG-specific B cells accelerate and exacerbate EAE, but are not able to induce spontaneous disease or demyelination without induced EAE |
| Stefferl et al. (87) | 1999 | Major histocompatibility complex (MHC) and MHC-linked effects can influence the antibody response and thereby disease severity in MOG-induced EAE |
| Lyons et al. (90) | 1999 | B-cell-deficient mice immunized with MOG35–55 induced EAE but not mice immunized with recombinant full-length MOG |
| Forsthuber et al. (88) | 2001 | MOG peptide 97–108 is the immunodominant human leukocyte antigen (HLA)-DR4-restricted T cell epitope in transgenic mice and is presented by human B cells expressing HLA-DR4 (DRB1*0401) |
| Lyons et al. (91) | 2002 | MOG-specific B cells and serum reconstitute the ability for inducing inflammatory EAE effects in B cell-deficient mice |
| Fillatreau et al. (93) | 2002 | IL-10 production of B cells regulate type 1 immunity and play a key role in EAE recovery |
| Svensson et al. (96) | 2002 | B cell-deficient mice with different genetic backgrounds (C57BL/10 and DBA/1) immunized with MOG1–125 showed decreased demyelination but inflammation was not affected |
| Bettelli et al. (97) | 2006 | TCRMOG × IgHMOG mice develop severe EAE, with inflammatory lesions in the spinal cord and optic nerves |
| Pollinger et al. (78) | 2009 | Transgenic mice expressing MOG92–106 specific T cells expand endogenous MOG-specific B cells, producing conformational, (epitope independent) Abs, and enhancing demyelinating EAE in a relapsing-remitting EAE model |
| Molnarfi et al. (94) | 2013 | MOG-specific B cells play a critical role in the EAE pathogenesis due to its function as an antigen-presenting cells |
| Parker Harp et al. (95) | 2015 | B cells directly interact with dendritic cells and enhance CD4 driven EAE severity in mice |
| Flach et al. (58) | 2016 | MOG-specific B cells accelerate MOG T cell driven EAE inflammation and disease severity |