A Little Poisoning Along the Road to ME/CFS
Looking at my symptoms, many of which are far less these days and some are gone, it would be easy to figure that I'd just been dealing with some heavy-duty menopausal issues.
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Altered functional B cell subset populations in patients with chronic fatigue syndrome compared to h

Discussion in 'Rituximab: News and Research' started by Firestormm, Mar 14, 2013.

  1. Firestormm

    Firestormm Guest

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    August59 and heapsreal like this.
  2. Firestormm

    Firestormm Guest

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  3. Ema

    Ema Senior Member

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    "Patients with CFS do not have hypogammaglobulinaemia, predisposition to recurrent bacterial infections or symptoms of autoimmunity."

    How did they determine this, I wonder?

    It certainly doesn't fit my profile at all considering I have all three.

    Ema
     
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  4. Mark

    Mark Acting CEO

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    Really?

    1988
    (PO Behan, WMH Behan. Crit Rev Neurobiol 1988: 4:2:157-178)

    (Anthony L. Komaroff. Chronic Fatigue Syndromes: Relationship to Chronic Viral Infections. In: Persistent Herpes Infections: Current Techniques for Diagnosis; Ed: Gerhardt RF Krueger, Dharham Ablashi and Robert C Gallo, Pub: Elsevier Press 1988)

    1989
    (The CFIDS Chronicle, Spring 1988)

    1992
    (Professor Nancy Klimas, A Physician's Forum - CFIDS: The Diagnosis of a Distinct Illness: The CFIDS Association, September 1992)

    ...etc etc...

    2011
    (Dr Gordon Broderick. http://www.research1st.com/2011/10/21/broderick)
     
  5. lansbergen

    lansbergen Senior Member

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  6. Gemini

    Gemini Senior Member

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    Mark, like your historical references & would add:

    1990

    "Alterations in the humoral response of patients with CFS have been found...These aberrations might represent polyclonal B-cell activation, as EBV is a potent polyclonal stimulator of B-cells(2). We found elevated B-cells, including B-cells that expressed the T1(CD5) marker, a subset that has been reported to be elevated in patients with autoimmune disorders(19). B-cell activity is regulated by an intricate balance between T-helper and T-supressor lymphocytes, as well as by NK cells. The depletion of the CD4+CD45RA+ Tinf cell subset in our patients may favor an alteration of B-cell regulation as a result of inactive suppressor cells. The NK cell deficiency observed in most subjects would also contribute to B-cell regulatory disturbance, since a primary physiologic role of the NK cell is thought to be B-cell regulation(1).

    (Immunologic Abnormalities in Chronic Fatigue Syndrome, Klimas N, Salvato F, Morgan, R, Fletcher, M, Journal of Clinical Microbiology, June 1990.)
     

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