Barts MS at ECTRIMS 2017


In just over a week, MS researchers, Nurses and Clinicians will travel to Paris for the annual ECTRIMS conference. This is an important meeting where new research, trial results and treatment information is shared across the community. And we’d like some input from you, our readers!

For the past few years, the Barts MS team have tried to get this information out to the readers of the this blog as quickly as possible. 

We have a range of activities over the three day event; posters, stands (Digesting Science and Clinic Speak), presentations and social media sessions. So again, we invite you to get involved!

Ways to get involved in the Burning Debate:

The aim of the Burning Debate is to get two top researchers to discuss a burning topic from the field of MS Research. This year the topic is: Rumble in the Jungle: B cells vs. T cells. Our two speakers will argue over whether MS is a T-cell mediated disease and if B-cells are therefore less important. 

The debate will take place on Thursday 26th October from 3.45-4.45pm in Hall D. 

We have Dr David Hafler arguing FOR the motion and Dr Stephen Hauser arguing AGAINST. The debate will be chaired by Dr David Wraith. Unfortunately the debate will not be live streamed, but we will be covering it on Twitter where you can follow the discussion by searching for the hashtag #burningdebate. A twitter feed will be projected in the debate room, so any comments or questions will be voiced. 

At the end of the debate, the BartsMSblog twitter account will post two tweets, one FOR the motion, one AGAINST. The tweet that is re-tweeted the most will win the debate. A secondary aim of the debate is to encourage clinicians to use Twitter in their professional capacity. 

Ways to get involved in the Hangout:

The aim of the Hangout is to get MS research presented at ECTRIMS out to you ASAP. Two of our best presenters, Neuro Doc Gnanapavan and MouseDoctor will be presenting live for one hour on Friday 27th October from 3:45pm – 4:45pm , summing up what they have seen throughout the week. This was our video from last year.

This is a great opportunity for you to find out about specific presentations that you’re interested in. Check out the conference programme here, and either email us or post a comment on this article with any sessions or posters that you would like to know about, and we can try our best to send someone there and will report back in the Hangout. 

So, you can either watch the Hangout on the Barts MS Blog google+ channel, on our You Tube channel or sign up and join the discussion. As this is a Hangout On Air, lots of people can watch the discussion but only 10 people can join and ask questions. If you join the discussion (rather than just watch the video live), your camera will be turned on so if you want to remain anonymous, it’s maybe better to email us your question. If you would like to be invited to join the discussion and be notified when the discussion starts, email us your details: We’ll also be checking our twitter, so you can tweet us a question on the day.

About the author

Alison Thomson


  • Hi

    I have question.

    If MS is completely B mediated disease, Then Brain Atorpy should normalise very quickly. Or as long as old plasma cells live. Is this happening with Ocrelizumab? If not, why Not? And does this imply 2nd or 3rd mechanism of neurodegenaratiin as yet not defined?

  • I would never say it is completely B because B do not appear in a void.

    Brain Atrophy is a problematic measure because is is a composite of nerve damage and swelling however I believe it should do similar stuff to alemtuzumab if it doesn't in a like for like situation then something else is happening

    • My point exactly. Question for ECTRIMS/ACTRIMS? If no one knows at least admit alemtuzumab is doong something more than b mediated drugs? So ms patient can at least choose with full knowledge what treatment is right for them?

    • We should do head to head and see if ocrelizumab in early MS give brain atrophy protection but unless the regulators pull their finger out and get ocrelizumab licensed I suspect we will never find out

  • In light of Barts blog view this is like trying to salami slice MS In many diseases
    Are you promoting just that ? MS being a B cell or t cell?
    If you look at the immunme system you know that all those cells are working (even inateimmunity) toghether so why split MS b or ms t disease …Have you ever wonder that In the end you both maybe right
    It remind me about the light theory some saying that light was a particle and others a wave….In the end they where both right
    PS: best of luck to all In the Ectrims 2017

    • In the immune system….no cell works in isolation and you don't get B cells without T cells,and you don't get T and B function. However as you know the MS blinker is firmly focused on the fact that T cells do every thing.

      If those blinkers come off…I suspect we will get more progress. I think pharma are ahead of the curve iin

      Ocrelziumab turns this view on its head and I think most people who work on EAE do not even register the B cell involvement.

      This debate pitches three immunological heavyweights (Wraith is a T cell biologist), Hafler used to be Mr MS T cell and Hauser is the self-acclaimed B cell guru.

      As long as they do not go into this B cell present antigen "love-in" it could be a good debate, Hafler has history on his side, Hauser has response to therapy.

      I know how I would approach this, if fact this is just as well as ProfG has volunteered me to do a debate on a similar subject "To B or not T-B that is the question" in London (yep I get to travel alot) where there is an absolutely fantastic list of speakers and hopefully we will hear about whether spontaneous EAE occurs due to knockout of a gene in B cells

      If the B cell is the major player then there are a load of new targets to test like the proteosome inhibitor you suggested. PLC G2 could be another

    • " B cell present antigen "love-in"
      "Hafler has history on his side"
      "I know how I would approach this.."

      Please explain…

    • In the past when we have had some American debaters they have steered clear from confrontation and have ended their arguments in a common place…hence the love-in where everyone is happy and smiley and everything is amazing.

      The common ground is b cells presenting to T cells if this road is taken it could be a non event

      Prof Hafler was at the leading edge of T cell biology. He and many, many others have pioneered the central role of T cells in autoimmunity. So the history of MS is all T cell.

      What would I do?

      My opponent may be reading so best not disclose my tack…I don't think to quickly so I'm not a good debater. I only agreed to do it so I would get entry into the meeting. Hope I don't swear 🙂

  • I love this idea. Bravo!

    Now I just have to get Gavin to take me seriously in suggesting the Smartphone Metric for cognitive function.

    If I am asked will I will say more

  • The Rumble in the Jungle will be very polite and the conclusion will be "not enough evidence yet…. more studies required". The idea that such a debate will result in a definitive answer is ludicrous. MS Research is an industry with a philosophy of expand or die. Even in Team G the number of Muse Doctors has increase by 50% (and Team G moans about austerity. ECTRIMS is a nice get together for MS Researchers and Doctors who will eat well, drink well and enjoy Paris. I'm not expecting any major breakthroughs to be announced – nothing to stop the ever increasing number of MS conferences. Why kill the goose which lays the golden egg? MS is a researchers idea of heaven – job for life.

    • Glass half empty then?
      Re the debate, at least the debate has now started, acorns oaks sorta thing.
      Re ECTRIMS Some of us have to stay behind and look after the mice whilst colleagues communicate their latest (outstanding) research.
      You may not believe it but for us MS researchers, our idea of heaven is the end of MS and it's not a job, it's more of a vocation.

    • MD2 – I'm just a realist (person with MS). This year is the 33rd ECTRIMS Congress. We should be further along than having a debate as to whether a T cell or a B cell is the main culprit. Prof G's novel (please tell him to stick to his dayjob as it's depressing stuff and he's no Barbara Cartland) shows how little progress has really been made. Tablet / injection to stop further deteriration is all we are after, but the ECTRIMS congress will be handing out prizes to a researcher who has injected mice with Coconut Milk combined with Copaxone. Please take care of the mice when the team are in gay Paris.

    • When I started working on MS, the only treatment for a relapse was steroids. Now there are multiple choices, at least for relapsing remitting disease. Identifying the main culprit in the immune system which seems to be the memory B cell, from MD's diligent research enables these to be targeted more specifically whilst sparing the rest of the immune system, which surely is a good thing.
      I take your point regarding stopping further deterioration, I've been working on neuroprotective agents for just such a purpose for a long, long time. The lack of progress to the clinic is a source of frustration and depression to me as well. We just can't seem to get pharma interested, I'm not a clinician so have no clout but you certainly won't unless you get to talk to them at these sort of meetings. I know you think these meetings are jollies (and they are for some of our more detached clinical colleagues, excepting team G of course!) but believe me, they're hard work at least for those who want to push things forward.
      Rest assured the mice will be in safe hands.
      Hugs and kisses

    • Mouse models of ms and the mouse drs that exist in a circular, insular and to date, fruitless world – are on a merry-go-round that is ineffective to those who live with ms.

    • I beg to differ, I am rather proud of our successes of moving ideas from the mouse into humans.

      I do not feel we are insular or fruitless, but is your ire vented at others?

      Our ideas have already proven to be effective in MS, on a number of occasions.

      Most basic scientists will never have the pleasure of moving an idea into the clinic

    • Do we need to have the same conversation every time ECTRIMS rolls around? The “mouse models are imperfect and they only serve to bring less than adequate therapies to MS patients at a huge financial windfall for Pharma” is tiresome, Let’s focus on what needs to be done I.e. neuroprotection\restoration using pharmacological, cellular,antiviral or genetic engineering techniques. New therpies need to penetrate the CNS and exert their effect beyond the periphery.

    • Well said Adam.

      Also you should understand that a purpose of these sessions is to engage neurologists with social media.

      Last week we had the good news that clemastije protest remyelination and I suspect people will be inundating their neurologists for prescription requests.

      Where searching questions asked.

    • But is it safe to take such high dosage of Tagvir. 4 pills in the morning, 4 in the afternoon to replicate the trial findings. Given it's only phase 2, and involves 50 patients. Same size as the trial taking Lipoic acid, but a lot safer bet. Granted particular optical isomer version. At least your reducing brain atrophy by 68%. So the trial says.

    • Also these findings were reported in AAN in 2016. It's just published in a peer review journal. Remember Ant lingo also had positive result in optical neuritisos but called miserably in phase 3. Given complex chemistry involved on brain repair. Just seems too good to be true.

    • "whilst colleagues communicate their latest (outstanding) research"

      … Sorry did I miss something? Was that perspective proffered by people show actually live with ms? Or is that just the view of the people who do the research?

  • Peripheral T-cells vs peripheral B-cells should not be the debate. Obviously both are "foot soldiers" and contribute to RRMS. MD is seemingly correct, with his extensive and convincing publication, that an effective RRMS therapy is based more on its ability to inhibit the B-cell response.

    The biggest question that seems to elude researchers is what is the antigen presenting cell (APC) that is calling this onslaught or relapses in MS and perhaps progression? Is it EBV controlled B-cells in follicles in the brain or is it hot microglia or is it A1 astrocytes? What causes the "field effect" when GIlenya and Tysabri are withdrawn or when the MS patient has an infection causing a relapse in the identical area of the brain or c-spine that was previously injured in an attack?

    It seems as though researchers are "stuck" on the effect (peripheral B-cells + T-cells) instead of the cause of MS (the antigen presenting cell) and this is probably why we have all therapies with NEDA outcomes of less than 50% (except HSCT) as we have not eliminated the cause sending out the signals to the peripheral immune system to then attack.

    • If it antigen presentation in the brain it is the perivascular microglia, simple. Astrocytes are not effective antigen presenting cells, people wasted half their lives on this thirty years ago.

      The question is what do you do about it?

      Insects live quite happily without any lymphocytes but can you live without macrophages, I wonder. The question is how do you target microglia and can this be done without affecting macrophages elsewhere and if so for how long should you target them. It can be done in mice, but I wonder how safe this will be in humans.

  • Thanks for you thoughts MD.

    I look forward to the Ibudilast trial results at ECTRIMS, which prevents glial cells from being activated, although I know you think PDE-4 inhibitor results will be negative. I am not really sure why these "hot" microglia could not be studied in detail in vitro and turned off or down-regulated as to not attract the peripheral immune system, especially B-cells?

    • I think the issue is how do you turn off the microglia without turning off macrophages elsewhere in the body. However the experiment may have already been done minocycline was supposed to be an inhibitor of hot migroglia, sodium channel blockers are supposed to block microglia, Laquinimod may do the same.

      In EAE I do not think hot microglia are being studied in the right way as the experiments are too short.

      Also I would say without using multiple approaches to target the issues in MS, we will not really see the benefit.

      We will know what happens to ibudilast…I've heard no rumour

    • "and this is probably why we have all therapies with NEDA outcomes of less than 50% (except HSCT) as we have not eliminated the cause sending…"

      Well said!

  • According to one of the presentations lemtrada more effectively treated relapsing ms. Does this not kill the B mediated theory of MS? Granted b cell highlight targets for t cells to attack. But how can one time treatment to b cells best a b cell treatment given every 6.months that is 10 times more potent than ritximab! I'm no t cell or b cell loyalist. Just pointing at data saying something else. I asked the first question on this article and hope this question is asked at ECTRIMS/ECTRIMS 2017.

By Alison Thomson



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