Why may alemtuzumab stop working in some people?


Have you ever noticed that when you have dandelions growing that if left to themselves you get long stemmed flowers, however if you cut the grass alot what you get are very short stemmed flowers

One thing to come out of the lockdown is the going to be a lack of EAE experiments as these are considered non-essential during the COVID-19 crisis. Inddeed we were stopped from doing such experiments even before the lock-down. Therefore how are you supposed to do your work?

Anyway below we have a paper of CD52 depletion in mice and it shows that alemtuzumab is an anti-B cell reagent which we know already, but it also may point to a reason why you can get relative treatment failure as we know that about 50% of people treated with alemtuzumab relapse. In the work below they show that when you deplete cells, they repopulate with cells that no longer have the CD52 on their surface. Now the paper below suggests that these cells may be regulatory and thats why it works so long, playing develis advocate this could mean that they will no longer be killed by CD52 and therefore you can have alemtuzumab treamtent that does work. Well that may be one reason, but Dr Angry is about to show you another reason…The count down is comming we are about to get the Irony of Alemtuzumab Part VI.

However, this is an interesting one and begs the question is this a phenomenon of selecting targeting negative cells when you repeatedly deplete lymphocytes.

OK you don’t want to read this stuff so back to the COVID19 stuff:-(

Anti-CD52 blocks EAE independent of PD-1 signals and promotes repopulation dominated by double negative T cells and newly generated T and B cells. Haile Y, Adegoke A, Laribi B, Lin J, Anderson CC. Eur J Immunol. 2020 May 10. doi: 10.1002/eji.201948288. [Epub ahead of print]

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Leave a Reply to luis fernando Cancel reply

  • they repopulate with cells that no longer have the CD52 on their surface

    I thing they are saying that T cell that dont have cd4 or cd8 markers are increased while b cells expresing cd 56 also increased

    “A substantially increased frequency of DN T cells was recently identified in MS
    patients treated with fingolimod [61], suggesting both a clincal relevance of our findings and that
    multiple treatments of CNS disease preferentially spare DN T cells. DN T cells may arise from the
    thymus or may be generated in the periphery due to loss of either the CD4 or CD8 co-receptor on SP
    T cells [62-64]. Loss of CD4 can be caused by chronic antigen stimulation [65]. While the proportion
    of DN T cells increased post anti-CD52, there was only a small transient increase in the proportion of
    DN T cells that were newly generated. This suggests pre-existing DN T cells either had increased
    survival or increased proliferation compared to CD4 and CD8 T cells, or that co-receptor expressing
    cells had downregulated their co-receptor.”

    • Yes you are right they were talking about T cells, I took their results into a direction. They have not considered

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