B cells are important in MS


B cell rich meningeal inflammation associates with increased spinal cord pathology in multiple sclerosis. Reali C, Magliozzi R, Roncaroli F, Nicholas R, Howell OW, Reynolds R. Brain Pathol. 2020. doi: 10.1111/bpa.12841. [Epub ahead of print]

Many years ago this group looked in the brain and reported that those people with B cell follicles accumulated grey matter damage to the brain. Now they move down the nerve and examine what happens in the spinal cord. They suggest that in people with B cell follicle-like strucutres there is more damage to the spinal cord also.

Therefore the idea of MD2 on progression still holds weight. The only way to work out if B cells in the CNS are important and that is to get rid of them. Will NDGs trial ever get off the ground?

Increased inflammation in the cerebral meninges is associated with extensive subpial cortical grey matter pathology in the forebrain and a more severe disease course in a substantial proportion of secondary progressive multiple sclerosis (SPMS) cases. It is not known whether this relationship extends to spinal cord pathology. We assessed the contribution of meningeal and parenchymal immune infiltrates to spinal cord pathology in SPMS cases characterised by the presence (F+) or absence (F-) of lymphoid-like structures in the forebrain meninges. Transverse cryosections of cervical, thoracic and lumbar cord of 22 SPMS and 5 control cases were analysed for CD20+ B cells, CD4+ and CD8+ T cells, microglia/macrophages (IBA-1+), demyelination (myelin oligodendrocyte glycoprotein+) and axon density (neurofilament-H+). Lymphoid-like structures containing follicular dendritic cell networks and dividing B cells were seen in the spinal meninges of three out of 11 F+SPMS cases. CD4+ and CD20+ cell counts were increased in F+SPMS compared to F-SPMS and controls, whilst axon loss was greatest in motor and sensory tracts of the F+SPMS cases (p<0.01). The density of CD20+ B cells of the spinal leptomeninges correlated with: CD4+ T cells and total B and T cells of the meninges; with the density of white matter perivascular CD20+ and CD4+ lymphocytes (p<0.05); with white matter lesion area (p<0.05); and the extent of axon loss (p<0.05) in F+SPMS cases only. We show that the presence of lymphoid-like structures in the forebrain is associated with a profound spinal cord pathology, and local B cell rich meningeal inflammation associates with the extent of cord pathology. Our work supports a principal role for B cells in sustaining inflammation and tissue injury throughout the CNS in the progressive disease stage.

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  • Yes they are. So are T cells. But until you explain why Ocrelizumab kills 99% inflammation but brain atrophy is poor. Also why alemtuzimab hsct are the most effective therapies not b only treatments. Ofatumab in brain atrophy was worse then aubagio. Then your not really moving field of ms research. And the cohort for alemtuzimab as younger does not cut it.

    • Dos not cut it…Why not….?
      If you can explain why not, then I will either counter your argument or change my mind but blind faith does not cut it either.

      Cladribine in MS 9 years post onset and cladribine = ocrelizumab 6 years post onset prbably = ofatumumba 6 years post onset…Optic neuritis (6 months before MS diagnosis) and cladribine = HSCT or alemtuzumab…Compare apples with oranges and you get turkeys.

      Swedish atrophy data with rituximab is as good as alemtuzumab…whilst I am happy to buy the idea of T cells and it would have to be CD8 T cells, you ask where is the data as opposed to Rhetoric.

      Yes I am being Devils advocate…but if no-one does this you simply buy into the the endless tosh that has dogged science for a long time.

      • Firstly I am no way stating a fact.just opinion. The reasoning behind this also swayed by talking To my neurol9gist and Ms nurse. Both say the same thing those treated with ocrelizumab do worse than those on alemtuzumab even if they suffer more side effects. This is probably.one of the top ms clinics in England only 2nd to bars with over 700 ms patients.

        • Experienece is a good thing if that is what it is as opposed to reading the trial papers, but you talk to neurologists and they say cladribine causes cancer….shit sticks. However, just because a clinic sees alot of pwMS may not mean it is on the ball….some places only prescribe beta interferon…yes I am being facetious but you get the point.

      • Also time of ms diagnosis is not equal to length of ms duration. Also rate Ms progression varies from person to person. So saying.a younger cohort is a red herring. Only the effect of drug vs.placebo is meaningful indicator. Probably age.of patient at start of.trialn9s.more.meaningful to.compare trial outcomes

    • Please define “poor”. Look at Phase 3 trial data. At 4 years of continuous ocrelizumab therapy, the whole brain atrophy rate is 0.4%, which is the higher end of normal for general population.

  • “Our work supports a principal role for B cells in sustaining inflammation and tissue injury throughout the CNS in the progressive disease stage”

    Then why does rituximab/ocrevus not stop ms progression..?

      • Swiis cheese BBB only works (or unworks ) for some studies


        Does an immune cell is smaller than an antibody?

        Acording to the wikipedia

        An antibody is about 10,nanometers

        B cell (Small lymphocytes) 7–8 micrometers= (7000-8000 nanometers)

        So B cell is about 800 times bigger than antibodies

        So why does one 800 bigger object gets in the brain easier than one 800 times smaller?

        Strange world




        • Not surprsing really when Plasma cells do not express CD20, the flow of intrathecal is away from the brain and as for how much complement and any cells involved in ADCC are in the brain used fro rituximab to kill B cells, is it surprsng that a few minutes after it was injected it was clearing the B cells out of the blood and not the brain. Don’t have the bad idea once, but repeat over and over again and now some bright spark says lets put it into the ventricles…so its OK to drill holes in peoples heads when 5 minutes of thinking says the chance of you achieving what you want to achieve is so low…It’s desparate

          • ” few minutes after it was injected it was clearing the B cells out of the brain and not the brain.”

            So if i understand right the antibody (rituximab ) cant enter the brain

            Butif you put it in the brain directly can leave in just a few minutes

            Strange world (Again)


            Ps: I have read that study some moons ago


          • Thanks edited to blood not the brain.
            When injected via blood very little antibody reaches the brain max 1%. The CSF drains into the blood

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