Discussion in 'Rituximab: News and Research' started by Firestormm, Mar 14, 2013.
"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.
(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)
(The CFIDS Chronicle, Spring 1988)
(Professor Nancy Klimas, A Physician's Forum - CFIDS: The Diagnosis of a Distinct Illness: The CFIDS Association, September 1992)
(Dr Gordon Broderick. http://www.research1st.com/2011/10/21/broderick)
For who wants to know more about Bcell populations
Mark, like your historical references & would add:
"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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