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Crowfunding for a study about etiopathogenesis and try to set potencial biomarkers

Discussion in 'Fundraising' started by Notjustfatigue, May 11, 2019.

  1. Notjustfatigue

    Notjustfatigue Established Member

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    Dear mates,


    I want to inform about a crowfunding campaign for a study about etiopathogenesis of ME/CFS that could lead to set potencial biomarkers for the disease.

    The current objective is of 46.800,00 € and the link for donations is the following:

    https://helpify.es/comunidades/todo-por-la-causa-del-sindrome-de-la-fatiga-cronica/

    All you have to do is to click on "DONAR" button and then just put an amount in the field "Donación" (this amount would be in € - you make conversion from $ to € here: https://fx-rate.net/calculator), fill your full name in the field "Nombre y apellidos" and your email in the last field. Then you just need to choose a payment method (Credit Card or Paypal) and proceed.

    You must also mark the checkbox "Acepto los Términos y condiciones y la Política de privacidad" (i accept the terms and conditions including the privacy policy) and in case you prefer to make an anonymous donation mark the checkbox below "Donar como anónimo" (donate as anonymous")

    I translate the message of the campaing and also take this opportunity to ask you for support in all means possible (if you can´t or don´t want to donate, you can just share in your social networks, email this post to contacts, etc).



    All for the Chronic Fatigue Syndrome cause


    How do you feel when there's no solution to a problem? You may experience sadness, helplessness, disappointment, failure, anger, fear, or even misunderstanding. That's why we're here. We want to find a solution for Chronic Fatigue Syndrome.


    The initiative comes thanks to Manuel Ruiz Pablos, a patient suffering from this disease, and his girlfriend Rosario Montero Mateo. Manuel's life was like that of any other university student, student of Medicine, who is enjoying one of the best stages of youth: travel, friends, sport ... And suddenly one day woke up with what seemed a cold. His life changed completely. After spending a lot of time from doctor to doctor and with unexplained chronic fatigue, he was finally diagnosed with Chronic Fatigue Syndrome. He tried to continue the degree but the symptoms made it impossible. Since then, together with Rosario, who is currently preparing the medical internship, both fight and study to find a cure for this disease. They have it clear: "we want the people who suffer it to recover their lives".


    Chronic Fatigue Syndrome or Myalgic Encephalomyelitis is a chronic disease that leads to physical fatigue and impaired cognitive capacity. It presents neurological, immunological and endocrine alterations. It lasts for weeks or even months. It is not relieved by rest and may incapacitate the patient. The person suffering from this disease may feel like an old man unable to move because of the pain he suffers.


    It is untreated and its cause is unknown. Drug treatments try to alleviate its many symptoms and other co-morbid diseases. This is one of the many reasons why CIMA has decided to undertake research into the cause of this disease in order to treat it effectively.



    We have a hypothesis to start with:

    Several investigations have demonstrated the presence of potential biomarkers that would indicate inadequate immune function and signs of autoimmunity as well as alterations in NK, cytokine profiles and T-cell response capacity. Therefore, we propose this hypothesis: patients with Chronic Fatigue Syndrome may have an alteration in the activation of T lymphocytes caused by a decrease in the HLA-II antigenic presentation due to intracellular pathogens.


    Symptoms

    ME/CFS usually begins with an infectious process in a commonly active person, which begins with fever, cough, odynophagia, myalgia... i.e., flu-like symptoms. From this onset, a permanent exhaustion is established that does not improve with rest. It worsens with both physical and mental activity that becomes persistent. When chronic symptoms are established, fatigue, febricula or temperatures of 35ºC predominate when the disease is more advanced. Also arthralgias, myalgias, cervical adenopathies, intestinal symptoms, increase in respiratory allergies, hormonal alterations... etc. It should be noted that all these symptoms are not present in all patients.




    Thanks in advance!!!



    Best :hug:
     
    Last edited: May 11, 2019
  2. Andy

    Andy Committee Member & Outreach

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    Who, or what, is CIMA? As far as I can tell this is who the funds raised would go to?
     
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  3. Notjustfatigue

    Notjustfatigue Established Member

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    Sorry about that. My fault.

    Yes, effectively the funds would go to CIMA.

    CIMA is the acronym of Centro de Investigación Médica Aplicada de la Universidad de Navarra (Applied medical research centre of the University of Navarra) which is a research reference center of our country, Spain.

    I left two links, one from its website in english and another one from wikipedia that you can translate with google translator:

    https://cima.unav.edu/en/

    https://es.wikipedia.org/wiki/Centro_de_Investigación_Médica_Aplicada


    Best :hug:
     
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  4. Sasha

    Sasha Senior Member (Voting Rights)

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    Hi @Notjustfatigue - So is the call for donations solely based on a medical student saying:

    "Several investigations have demonstrated the presence of potential biomarkers that would indicate inadequate immune function and signs of autoimmunity as well as alterations in NK, cytokine profiles and T-cell response capacity. Therefore, we propose this hypothesis: patients with Chronic Fatigue Syndrome may have an alteration in the activation of T lymphocytes caused by a decrease in the HLA-II antigenic presentation due to intracellular pathogens."​
     
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  5. Trish

    Trish Moderator Staff Member

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    Hi @Notjustfatigue. I am concerned that this crowdfunding is too vague. In its present form I can't see it as something I would want to donate to, or ask others to donate to.

    There is no detail about who will do the research, what they intend to do, or how they intend to use the money. The statement on the crowdfunding page, at least in the English translation does not come across as a professional fundraiser for a planned project, more as a couple of individuals who want to collect money in the hope that someone at the University will do some research if there's money for it.

    I am more accustomed to being asked for funds by recognised charities like OMF, Solve, The ME Association, etc. who not only give money to research, but scrutinise the planned research to judge whether it is a valuable and viable project. Or alternatively, research teams already working on ME, such as the UKME Biobank, raise funds for specific purposes.

    Please can you give us a link to something from researchers at the University with their plans for the research. Otherwise, I am sorry, I simply don't know whether this is for real or a scam.
     
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  6. arewenearlythereyet

    arewenearlythereyet Senior Member (Voting Rights)

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    I’m not sure this is a very specific hypothesis. There are many who inconveniently do not start like this just going by anecdotal accounts and up to 50% from some studies have gradual onset if I remember rightly. To not even acknowledge this is a bit of a red flag.

    You could argue that onset defines a sub-type but that also doesn’t seem to hold water when you look at how heterogenous the presentation of symptoms and severity is across the group.

    So even if the proposed research funding request was properly structured, vetted etc with an experienced biochemist/microbiologist to do the work proposed (whatever that is), then I probably still wouldn’t donate due to the hypothesis having a lot of holes in it.

    Sorry.
     
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  7. Notjustfatigue

    Notjustfatigue Established Member

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    Actually it came from that person's idea, along with his girlfriend (who has already finished medical degree) as a result of this study they did (i attach the study).


    @Trish I understand your concern about that and, in fact, I appreciate the caution, because it gives me the confidence that any initiative you support in S4ME can be worthy of my full confidence.


    These links explain who the crowfunding platform is and, as you can see, it is the University of Navarra itself and the CIMA mentioned above (they are in spanish language, but I think they're pretty understandable with the google translator.


    https://helpify.es/quienes-somos/

    https://helpify.es/preguntas-frecuentes/


    The principal investigator of the project is Doctor Bruno Paiva. His profile in Research Gate is the following:

    https://www.researchgate.net/profile/Bruno_Paiva2


    I don't know if there's anything else I can do so you can check the reliability of the project. I understand that the usual thing is to raise funds for entities such as OMF, SolveCFS, ME Action or well-known people within the community as is the case of David Tuller.

    In this case, as you can see in the logos below, despite having started yesterday, the campaign has already been supported by several patient organizations, among which SFC-SQM Madrid which is the largest association of CFS patients at national level in Spain and other important ones such as FibroProtestaYa or FRIDA.

    If you can guide me on what more information you would see necessary to be sure that it is not scam and decide to support and share the initiative, I contact them and try to expand the information.

    I have nothing to do directly (except that the secondary researchers, Manuel and his girlfriend are friends of mine) with the research or crowfunding and all I am just trying to do is giving the maximum possible dissemination for one of the few occasions in which a serious research project arises in our country.


    Sorry about not having known how to do it better. I will try to provide you all the information you need.


    Best :hug:
     
    Last edited: May 11, 2019
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  8. Trish

    Trish Moderator Staff Member

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  9. arewenearlythereyet

    arewenearlythereyet Senior Member (Voting Rights)

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    This still doesn’t explain what the proposal is ...?

    At least we have the lead researcher ...has he not written a proposal including an experimental design, proposed cohort, timeframe? Has he done a full literature search to back up his proposal and hypothesis (whatever that is).

    Surely there is more than this?

    I am increasingly worried that this campaign could be quite misleading if some of these key bits of information are missing.
     
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  10. Notjustfatigue

    Notjustfatigue Established Member

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    I have contacted my friend. I will try to answer some of the questions. He is going to consult with the lead researcher if he can provide any more details and which ones.



    The main purpose is to try to make an immune characterization starting from the hypothesis of an alteration in the activation of T lymphocytes caused by a decrease in the antigenic presentation HLA-II by B lymphocytes in the secondary lymphoid organs. This could lead to the establishment of potential biomarkers, which could serve to characterize at least one subset of patients.

    The proposed cohort will be 100 patients and 50 healthy controls and the estimated time since the provision of funds is obtained and the trial is completed is one year.

    Attached is the article (not yet published) that they first wrote before contacting some research centres until they found a researcher in one of the most prestigious research centres in Spain (CIMA) who was interested in and committed to the research project.

    I also leave a link to the profile of the lead investigator on the website of the University itself, as well as to the website of the University Clinic:

    https://cima.unav.edu/en/investigacion/plataformas/citometria/equipo/bruno-paiva

    https://www.cun.es/en/


    Hope this would be helpful.


    Best :hug:
     

    Attached Files:

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  11. Alvin

    Alvin Senior Member (Voting Rights)

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    Based on the first post the fundraiser's have a specific theory and expect that once they prove it we will have a disease mechanism. At this point thats simplistic, dozens if not hundreds of theories have come and gone and none have a solid compass saying look here and find the pot of gold. So while this theory may be correct the chances are it is not.

    This is analogous to saying we want to build a new widget and need kickstarter money. Once we raise enough the project can be built then proceed to mass production. This theory is nowhere near that stage.

    That said every realistic theory deserves looking into because if we get cynical and stop looking we will never find the answer and we have to accept we will go down hundreds if not thousands of dead end streets till we find the right one. But we have little money to go around, this is much like getting blood from a stone. If this theory fails to pan out then promising ones will have even less luck raising money.

    I would highly recommend looking into your country's medical research budget. They know the chances and risks of medical research though i don't doubt you would have a lot more trouble then well known diseases at getting funding.

    We are talking 52572.46 USD here. Half of what we just finished killed ourselves raising for David Tuller who can't get medical research funding.
     
    Last edited: May 11, 2019
  12. arewenearlythereyet

    arewenearlythereyet Senior Member (Voting Rights)

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    I’ve had quite a deep skim through the attachment. For those who want the proposal I would suggest skipping to the discussion at the end. I’ll try and summarise for those of us who are cognitively challenged.

    The main idea is that EBV is the root cause for at least a large subset of PWME and the study is to look into this.

    There is discussion about EBV infecting the CNS with what I think are some fairly tenuous links to patient cognitive dysfunction symptoms. There is also discussion about infection of epithelial cells and serotonin regulation linking this to IBS, gut sensitivity, cognitive dysfunction and sleep regulation problems. These links also seem fairly “top line” and theoretical. Not to say that these may not be a factor in some people but it seems a bit odd that PWME that don’t have an infectious route have these symptoms as well. There is no discussion about the millions of people who don’t have an acute infection at onset.

    He goes on to discuss heterogeneity in patients and their response to EBV infection

    And suggests that working out a classification of patient sub groups would be beneficial. Note this seems to have been proposed some time ago before the results of the rituximab study was known.

    However there is also discussion about another treatment using T cells to target EBV infected B cells.

    And here is a bit about what is proposed:

    But again this lacks the detail on how the cohort will be selected in the first place. There is reference to a Biobank on the university pages but I’m not sure what sort of criteria will be applied to select the sample.

    I’m still dubious about this, but as @Alvin mentions there is some use in studies that answer with a negative result.

    My main concern remains in some of the assumptions and lack of detail around experimental design.
     
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  13. Notjustfatigue

    Notjustfatigue Established Member

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    @arewenearlythereyet Thank you very much for the effort taken to summarize the attached so that colleagues with cognitive problems could become informed.

    AFAIK, the samples would not be taken from the Biobank.

    On Monday, my friend will ask the lead researcher whether he can provide the inclusion criteria and, if he can, as soon as he tells me them I will post them on the thread.


    Best :hug:
     
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  14. Binkie4

    Binkie4 Senior Member (Voting Rights)

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  15. Snowdrop

    Snowdrop Senior Member (Voting Rights)

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    Hello @Notjustfatigue

    Welcome to S4ME. My thinking on this is that if the people mentioned have an earnest desire to find solutions they may want to take a moment and rethink. I understand the urgency they may feel. ME is life altering.

    All of the people you mentioned whom we have donated to they had first already been working on the problem and we could assess their work. This includes D Tuller whom we just crowdfunded for. He started working on his investigation first.

    This is not a simple problem and I think if someone would like to work on research it would be a good idea to get up to speed by perhaps (for example) going to the Invest in ME conference in London.

    http://www.investinme.org/IIMEC14.shtml

    There would be opportunities to network and discuss ideas there. There is no need to necessarily start from scratch either as there is an ME biobank that may be willing to share samples for the right project. Or the university could contribute to some project already in the works if it is along the lines of the investigation being considered.

    https://cureme.lshtm.ac.uk/researchers/431-2/

    Apologies if you are already aware of these things. Just thought I'd provide some thoughts.
     
  16. Notjustfatigue

    Notjustfatigue Established Member

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    @Binkie4 That' s right, but in this case it is not about researching the b cells themselves, but about the low level of activated T lymphocytes that would indirectly indicate a decrease in the antigenic presentation of HLA-II.


    @Snowdrop Thank you so much for the welcome. Not only do you not have to apologize but I greatly appreciate your advice and insights.


    I think I misexpressed myself. That was precisely what I meant, that the entities or people to whom it was donated were people whose previous work was already known. I myself have donated for most of these causes, for some of them on several occasions, the last one precisely for the collection of David Tuller who does an impeccable work debunking the PACE trial and everything related to GET and CBT.


    I really do appreciate the suggestion about the IiME, but the main problem is that the lead researcher is not an exclusively ME focused researcher and, my friend, the promoter of the idea is a PwME and his girlfriend is a medical degree who is preperating the medical residency, so attending to the event, sadly, is not an option, at least this year.


    Thank you so much for the idea of the Biobank. This university already has its own Biobank, but the intention was to obtain specific samples for the study. I don't think that the economic amount would vary very much, given that blood collection is precisely the cheapest part of the whole process and the cost of sending the samples from London to Madrid under the right conditions is likely to even exceed that of the extractions.


    Nevertheless, I reiterate my total gratitude for the advices (they are always welcome) and I will pass them on to my friend so that they could serve him even if it was to get some idea out of them.


    Best :hug:
     
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  17. Dudden

    Dudden Established Member (Voting Rights)

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    Hello there @Notjustfatigue. From my understanding, this study i going to be conducted in Spain, correct? I am delighted that CFS has reached the interest of a university outside of America as well as some other countries. The hypothesis states that there is a possible "alteration in the activation of T lymphocytes caused by a decrease in the HLA-II antigenic", but how should "alteration" be interpreted? I am saying this due to the fact that an over-active immune system was proposed and even noticed many times earlier in CFS patients and not an under-active one. I am writing this solely for the purpose of clarification and the fact that if earlier studies proved a hypothesis correct, than maybe the university should shift it´s attention towards other possibilities and theories so the money would be used on useful discoveries and hopefully new breakthroughs. Please, dont missunderstand my intention, for I am not here to discredit the work but I am rather more concerned for it´s efforts to be wasted. We would then gladly fund these researchers.
     
  18. Manuel

    Manuel New Member

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    Good afternoon,
    I am Manuel Ruiz, medical student in Spain and I am sick with CFS/ME. Together with my girlfriend Rosario, graduated in Medicine from the Complutense University of Madrid, we contacted one of the best research centers in Spain, CIMA, to carry out the project described below.

    Currently I have seen quite a few lymphocyte typages that have provided me with CFS/ME patients. They could be grouped into two main groups:

    -In the first group they present reduced levels of total t lymphocytes (CD4, CD8, activated t lymphocytes) that indicate the presence of an immunodeficiency of T lymphocytes.

    -In the second group the patients have total t lymphocytes (CD4, CD8) and immunoglobulins in normal values. But this does not mean that there cannot be some type of cell immunodeficiency. The analysis of activated CD3+ HLA-DR+ and CD3+ CD4+ HLA-DR+ T lymphocytes is used to see if there is indirectly a decrease in the MHC class II antigenic presentation, since CD4 T lymphocytes are activated through this antigenic presentation made by B lymphocytes (antigen-presenting cells) in the secondary lymphoid organs. Therefore, if there is a decrease in the expression of class II histocompatibility molecules in B lymphocytes, they would not present antigens to CD4 T lymphocytes and these would not be activated. For any T-lymphocyte to be able to perform its functions and become an effector lymphocyte, it is necessary for them to be activated. That is to say, the values of the activated CD4+ HLA-DR+ T lymphocytes indicate indirectly if there is any problem in the class II MHC antigenic presentation made by the B lymphocytes.

    There is a congenital immunodeficiency called class II MHC deficiency in antigen-presenting cells, which is associated with a severe decrease in CD4+ (activated) T lymphocytes. This absence of cooperating T lymphocytes (CD4+) causes a deficiency in humoral response (the low number of CD4+ T lymphocytes causes a defect in collaboration between T and B lymphocytes) and cellular response (due to the intrinsic defect in the number of CD4+ T lymphocytes). Patients suffer repeated infections, particularly of the digestive tract. The genetic defect of this severe immunodeficiency is found in several proteins regulating the transcription of HLA class II genes.1

    Figure (photo attached): Regulation of class II HLA genes in normal individuals (above) and in patients with class II HLA deficiency (below).1

    The following are the ESID (European Society for Immunodeficiencies) diagnostic criteria for this congenital immunodeficiency:2

    A. Definitive diagnosis: if both criteria are met:
    • Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
    • Mutation in one of the genes: CIITA, RFX-B, RFX-5 or RFX-AP.

    B. Probable diagnosis: if all four criteria are met:
    • Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
    • Failure to thrive, opportunistic infections or persistent viral infections.
    • Normal number of T and B cells.
    • Normal proliferative responses to mitogens.

    C. Possible diagnosis: the first of the criteria plus at least one of the following:
    • Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
    • Hypogammaglobulinemia.
    • Normal mitogen responses but absent T cell proliferation to antigens.
    • Normal number of T and B cells.
    • Reduced number of CD4+ cells.
    • Failure of mononuclear cells to stimulate a mixed lymphocyte culture.

    The four genetic disorders that give rise to this congenital immunodeficiency are clinically indistinguishable. In most cases, there is no Class II expression. However, in others, the intensity of expression of MHC-II molecules may be as high as 5% of normal. Patients with higher expression tend to have a milder course of disease. These patients may survive beyond early childhood.3

    We believe that the difference between this congenital immunodeficiency and that found in the second group of CFS/ME is in the number of antigen-presenting cells that have class II MHC deficiency. In the CFS/ME group it would only occur in those cells infected (mostly B lymphocytes) with an intracellular pathogen and in congenital immunodeficiency is in all antigen-presenting cells.

    There are several intracellular pathogens that reduce the MHC class II antigenic presentation as an evasion mechanism of the immune system. The best known is the Epstein Barr virus, where it has been demonstrated that the latent protein LMP2A mediated the reduction of CIITA levels by decreasing the expression of PU.1 and E47 in B cells.4 Others such as human cytomegalovirus, human parainfluenza virus type 3, and varicella zoster virus suppress the IFN-γ-induced expression of class II MHC through inhibition of JAK-STAT activation and the transcription route activator, resulting in a reduction of CIITA expression.4 This may confirm the infectious origin of SFC/ME.

    Both groups of CFS/ME have a type of immunodeficiency and it appears that those with a total T lymphocyte immunodeficiency (not just activated) are in a more advanced stage of the disease, and those with only decreased activated t lymphocytes are in an early stage. Both justify the recurrent infections that these patients present and the chronic fatigue that they present.

    We spoke with Dr. Montoya and Dr. Ron Davis to see what they thought about our hypothesis. Both were interested. An immunologist from Ron's team told us that they could not carry out the study at the moment because they had several lines of research open and that it would take them a long time to start doing so. This is why we were looking for a research center where it could be done as soon as possible, because as a sick person I also want this nightmare to end. Dr. Bruno Paiva offered to help us but we had to raise the funds ourselves, as he did not have funds for this disease at this time.

    I hope you will help us with outreach and fundraising.
    I will try to solve all the doubts that I can.
    Greetings

    Bibliography.

    1. Regueiro González J.R., López Larrea C., González Rodriguez S. y Martínez Naves E. Inmunología: Biología y patología del sistema inmunitario. 4ª edición. Editorial Médica Panamerica, 2010.

    2. Serrano Martín MªM. , et all. Déficit de expresión de moléculas de clase II del complejo mayor de histocompatibilidad. Anales de pediatría. Marzo 2007. Vol: 66, nº3 pag:227-339. Available in:
    http://www.analesdepediatria.org/es-deficit-expresion-moleculas-clase-ii-articulo-13099694

    3. MHC class II deficiency diagnostic criteria. European Society for Inmunodeficiencies. Available in:
    https://esid.org/Working-Parties/Clinical-Working-Party/Resources/Diagnostic-criteria-for-PID2#Q10

    4. Jiun-Han Lin, Ju-Yin Lin, Ya-Ching Chou, Mei-Ru Chen, Te-Huei Yeh, Chung-Wu Lin, Sue-Jane Lin and Ching-Hwa Tsai. Epstein-Barr virus LMP2A suppresses MHC class II expression by regulating the B-cell transcription factors E47 and PU.1. American Society of Hematology. April 2, 2015. Col. 125 no. 14 2228-2238. Available in: http://www.bloodjournal.org/content/125/14/2228/tab-figures-only?sso-checked=true
     

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  19. Alvin

    Alvin Senior Member (Voting Rights)

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    Thanks for the additional information and welcome to the forum.

    Its interesting to hear you have spoken with two of the big players and they are both supportive. And its not incredibly surprising that they can't take on even more work at this time even if it is disappointing :(
    The biggest problems here are that we have been through with what sounds promising many times and been disappointed as well as we have trouble raising funds, being usually unemployed plus we just finished raising money for David Tuller as i mentioned earlier in the thread, in my case i had saved up extra money over the past year as a donation and would not be able to donate to your research.
    I did notice you have already raised some money which is good news but i had also asked earlier is there a way to get research money from your government's medical research budget (assuming there is one)?
     
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  20. Jonathan Edwards

    Jonathan Edwards Senior Member (Voting Rights)

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    Hi @Manuel,

    Good of you to come on the forum. As you may know, I am a retired professor of immunology with a special interest in B lymphocytes (and the use of rituximab). I understand your enthusiasm for looking for an immunological cause for ME but I am not sure things are as clear as you might propose.

    The first problem is that many people have looked at lymphocyte phenotying in ME and the consensus is that it is pretty normal. Even the NK findings have not been consistent. There have been some subtle T cell findings but not along the lines you suggest as far as I know.

    There has been a historical fashion for thinking that ME involves some sort of immunodeficiency, maybe by analogy with AIDS, but personally I cannot see any good reason to think that. People with ME do not get significant opportunistic infections and immune parameters are generally normal.

    The problem with studying blood lymphocyte phenotypes is that it is very hard to take into account shifts in compartmentalisation that occur with immune responses. Cells in the bloodstream are mostly the inactive ones with nothing to do on the way to somewhere where they may find something to do. The classic paradox is that if you give anti-inflammatory steroids the numbers of neutrophils in the blood go up because they do not migrate out into tissues - the same finding as you get with infection. I rather suspect that if anyone finds differences in lymphocyte populations in ME blood they are most likely to be due to a lack of physical activity reducing the baseline level of tissue inflammation and repair.

    I do not wish to discourage anyone from driving research forward but it would be a pity to focus in too hard in terms of expectations. More data on lymphocytes may one day provide a clue to what is going in ME but I would caution against trying to interpret findings in terms of a complicated predefined hypothesis. What is much more important is just finding something that everyone can replicate - and then trying to work out what it means.

    Best wishes

    Jo Edwards
     
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