More of the same….anti-CD20 inhibits seroconversion, but there is a T cell response. Even if there is an antibody response it is of lower quality. Get vaccinated before anti-CD20 and the vaccine response is like controls.
Time matters and the longer the interval between dose and vaccine more response.
So I think it is safe to say we know this already….but prepared this has not finished publication wise
The detection rate of COVID-19 in anti-CD20 treated pwMS (2.36/100 patient years) was similar to that of confirmed SARS-CoV-2 cases in the general Berlin population (3.75/100 person years) during the study period. In anti-CD20 therapy-naïve pwMS, it was 9.69/100 patient years
However remember the T cell immunologists were making a big case that anti-CD20 inhibits antigen presentation as a mechanims of action of anti-CD20 in MS..
Now also remember in these current studies there is no inhibition of the T cell response. You can’t have it both ways. So remember this when you think about what may be happening with regard to CD20 depletion and T cell activity in MS. It would seem logical that this activation pathway of an exogenous antigen being presented for T cell activation is not going to be driving MS, otherwise there would be no T cell response.
MS B cell Guru II would have it that CD8 T cells are important in driving MS based on their ECTRIMS 2021 late breaker, but in their Nature medicine COVID paper they show that T cell responses were not affected and indeed CD8 responses were enhanced. So how does that work? They will have to build their observation into their MS World, if they are to make head way and sense of what is going on.
Will they ignore the link and treat each piece of work as separate entity so they don’t need to have an MS World?
We on the other hand we can sit back and watch it unfold as we did not dig outselves into such a hole:-).
Is there an explanation…probably but let’s see if Guru II and the Immunology gang can come up with an answer.
COI None relevant
General Disclaimer: Please note that the opinions expressed here are those of the author and do not necessarily reflect the positions of the Barts and The London School of Medicine and Dentistry nor Barts Health NHS Trust and are not meant to be interpreted as personal clinical advice.
I don’t want to do whataboutery but I’m going to do exactly that 🙂 What about people on Fingolimod? Is there a Fingolimod exit plan or are us older people on Fingo destined to never go to a concert ever again?… I say this because I’ve just had to cancel a trip to London to go to a gig. Can’t risk the tube or just being indoors with lots of people and I’m feeling a bit fed up about it.
I’ve changed drug. I wasn’t just worried about covid but now I’m in my seventies I want the shingles vaccine.
To say that there is a t-cell response to Covid infection or vaccination that is not affected by B cells is heartening but there must be an inherent time line for entice duration of the T cell response. Will we talking about gaps in both B cell and T cell response? And will we talking about booster doses to coincide with (1) B cell repopulation (2) diminution of Covid antibodies and (3) diminution of T cell redpondivity. Doesn’t sound simple.
In humans immunity is for life once formed. Booster may increase the frequency of cells cable of responding. If they are not used they will wait but can come back when needed
“In Humanitas immunità si for life once formed”. Does that imply that an Ocrevus patient who got COVID once + two doses of Pfizer can consider herself protected, despite the lack of detectable anti-bodies? Thanks
If you had covid and recovered you will probably have sufficient immune protection to deal with it again on re-infection.
“For life once formed” Doesn’t sound positive for those of us with Autoimmune :)))
That is the basis of childhood immunity see the infection protected for life…so autoimunity will be no different…We can’t have it boths ways…unless you are a mouse then immunity does wane apparently