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]