#MSCOVID19 It’s not T-time is M-time. Alemtuzumab shows more evidence to support a major role for the macrophage

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You do not need peripheral B cells in the blood to fight COVID-19 so does that mean it is T-time for the T cells to get rid of COVID-19.

Woo, M.S., Steins, D., Häußler, V. et al. Control of SARS-CoV-2 infection in rituximab-treated neuroimmunological patients. J Neurol (2020). https://doi.org/10.1007/s00415-020-10046-8.

There are no B cells and no anti-SARS-Cov2 antibodies

If they had read our paper…… The underpinning biology relating to multiple sclerosis disease modifying treatments during the COVID-19 pandemic.Baker D, Amor S, Kang AS, Schmierer K, Giovannoni G.Mult Scler Relat Disord. 2020 May 12;43:102174. doi: 10.1016/j.msard.2020.102174. …..They would have known this.

Alemtuzumab is the sledge hammer to MS and it depletes your T and B cells and your MS goes away. So does your protective immune response, at least for a few weeks and this can be seen by the need to use treatments such as Acylovir to reduce viral infections. What happens to you when you get COVID-19..you may predict disaster…howeverwe have made the case that the innate immune response is numero uno when it comes to kicking COVID-butt. The clinical experiment will give us the answer and there are a few case reports that support this view and the best one has just surfaced.

COVID-19 and multiple sclerosis: A description of two cases on alemtuzumab Eva Fernández-Díaz, Julia Gracia-Gil, Jose Gregorio García-García, María Palao, Carlos M Romero-Sánchez, Tomás SeguraDOI: https://doi.org/10.1016/j.msard.2020.102402

In previous study an individual that recovered after getting COVID 2 weeks after alemtuzumab had low (paenic) white blood cells was lymphopaenic (90 cells /microlitre) and neutropaenic (75 cells /microlitre).

Was this a fluke?. Well you may remember a London Neuro thought they had a pwMS who had COVID-19 2 weeks after infusion. The problem was there was no confirmation.

However this is the best case report on alemtuzumab and says that lymphocyte levels in the blood can be essentially zero and you can still recover from COVDI19

multiple sclerosis: a description of two cases on alemtuzumab. There were zero lymphocytes at the time of infection and only 160 cells/microlitre which is grade 4 lymphopenia (below 200 cells/microlitre) compared to the lower limit of normal at 1000 cells/microlitre = 1,000,000,000 per litre of blood )

However let’s look at the innate immune (monocytes and polymophonuclear neutrophils (PMN) response

You can see that the innate immune response comes to the rescue, also you will notice that an anti-COVID-2 response is produced, just as I predicted.

Alemtuzumab is clearing the blood, but not the lymph glands one suspects,

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MouseDoctor

6 comments

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  • MD, what should the last sentence say? It looks like it’s been cut off… and I want to know what you believe it shows! Thanks 😊

  • Lollll

    Its not behind you anymore 🙂

    This
    means
    that
    some immunocompetence
    is
    maintained
    ,
    probably
    because the
    remaining
    lymphocytes are
    functional
    , the depletion in
    lymphoid organs is scarce and the innate
    immune response is mostly preserved
    ,
    since m
    acrophages
    ,
    NK cells
    and neutrophils
    have a low CD52 expression
    (Turner et al., 2013; Wray et al., 2019)
    .

    Macrophages are not tipicaly your antiviral cell from the innate immune system
    I would consider Nk cells (like the authors paper said)

    Actually they sometimes became Viral Targets and Reservoirs

    “Both acute and chronic inflammatory programming of macrophages can be utilized by viruses for their dissemination, replication and survival. M1-polarized cells are susceptible to viruses and they recruit other cell populations to the inflammation site, which favours virus transmission and dissemination. By contrast, M2 macrophages are involved in chronic disease and ensure permissiveness and the tissue distribution of viruses, forming a life-long reservoir of infection able to be activated and replenished upon conducive conditions.”

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6163364/
    Agradecido

    • The question for the NK is does it need antibody to be functional anf NK are not that common in the lesions. As for anti-viral Toll like receptor eight reacts to RNA virus and is present on macrophages

      • Tlr are present in an array of cells

        Dendritic cells, macrophages, natural killer cells, cells of the adaptive immunity T cells, and B cells, and non immune cells (epithelial and endothelial cells, and fibroblasts).[3]

        In recent years TLRs were identified also in the mammalian nervous system. Members of the TLR family were detected on glia, neurons and on neural progenitor cells in which they regulate cell-fate decision.[7

        They are part of and immune pathway beteween the inate an adaptive immune system

        Toll-like receptors have also been shown to be an important link between innate and adaptive immunity through their presence in dendritic cells.[6] Flagellin, a TLR5 ligand, induces cytokine secretion on interacting with TLR5 on human T cells.[6]

        They are dificult to change

        Because of the specificity of toll-like receptors (and other innate immune receptors) they cannot easily be changed in the course of evolution

        Thats why humsns have adaptive immunity (tailored to the pathogen and as memory

        https://en.wikipedia.org/wiki/Toll-like_receptor

        Tlr 8 Hiv/influenza virus

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