کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5630292 | 1580375 | 2016 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein Amelioration of EAE by a cryptic epitope of myelin oligodendrocyte glycoprotein](/preview/png/5630292.png)
- MOG61-85 represents a cryptic epitope of rMOG in wild-type C57BL/6 mice.
- MOG61-85 is naturally processed in B cell-deficient C57BL/6 mice.
- Immunization with MOG35-55 + MOG61-85 ameliorates clinical EAE in B cell â/â mice
- Processing of MOG61-85 is regulated by an antibody-dependent mechanism
Previous work demonstrated that EAE induced by recombinant human MOG was B cell-dependent. Data presented here reveal a T cell response to MOG61-85 in human rMOG-immunized B cellâ/â mice not observed in WT mice. Further study revealed this peptide to be a cryptic epitope in WT mice. Co-immunization of B cellâ/â mice with MOG35-55 and MOG61-85 peptides led to less severe disease compared to mice immunized with MOG35-55 alone. Disease amelioration was associated with decreased production of Interferon-γ by lymph node cells. Thus, MOG61-85 represents a protective epitope to human rMOG induced EAE in B cellâ/â mice.
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Journal: Journal of Neuroimmunology - Volume 300, 15 November 2016, Pages 66-73