کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5630252 | 1580372 | 2017 | 9 صفحه PDF | دانلود رایگان |

- Mice treated with murine anti-CD52 are protected against EAE disease progression.
- Synthesis of inflammatory cytokines is significantly suppressed following treatment.
- Enhanced IL-10 in plasma of EAE mice indicate treatment effect in periphery.
- Anti-CD52 treatment induces CD39Â + regulatory T cells in EAE mice and MS patients.
While examining the therapeutic value of anti-CD52 antibody against EAE/MS, we identified a unique subset of CD39Â + Tregs in repopulating GALT tissues, a major lymphoid reservoir, which was accompanied by amelioration of disease. Furthermore, anti-CD52 treatment leads to increased expression of BDNF, IL-10, and SMAD3 in the brains of EAE mice. This condition is associated with suppression of IL-17, a critical inflammatory factor in EAE/MS progression. Additionally, we found elevated levels of CD4Â +Â CD39Â + Tregs in PBMCs of RRMS patients treated with humanized anti-CD52 mAb. Thus, anti-CD52 can affect multiple immune mediated pathways involved in the pathogenesis of EAE/MS.
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Journal: Journal of Neuroimmunology - Volume 303, 15 February 2017, Pages 22-30