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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

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    Cornwall England
     
    August59 and heapsreal like this.
  2. Firestormm

    Firestormm

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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 Former 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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    August59 likes this.
  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    Mark, like your historical references & would add: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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