While examining the therapeutic value of anti-CD52 antibody against EAE/MS, we identified a unique subset of CD39+ 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 CD4+CD39+ 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.
Pant AB, Wang Y, Mielcarz DW, Kasper EJ, Telesford KM, Mishra M, Haque A, Smith J, Kasper LH, Begum-Haque S. Alteration of CD39+Foxp3+ CD4 T cell and cytokine levels in EAE/MS following anti-CD52 treatment. J Neuroimmunol. 2016 Dec 21. pii: S0165-5728(16)30286-7.
This paper looked and found an increase in a Treg population that goes into the Gut Associated Lymphoid Tissue (GALT). This is reported to increase in MS, so is this a reason why MS goes away?
Time will tell…however are we being sold a curve ball?…
Does it tell us about why alemtuzumab works or does it tell us how alemtuzumab causes autoimmune side effects.