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B-cell alterations in ME/CFS ‘may suggest subtle tendency to autoimmunity’

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www.ProHealth.com • December 4, 2012


Article:
Altered functional B-cell subset populations in patients with chronic fatigue syndrome compared to Healthy Controls
- Source: Clinical & Experimental Immunology, Nov 2012

By A.S. Bradley, B. Ford, A.S. Bansal

[Note: This article, abstracted below, is not yet available in formatted full text. The research took place at an NHS center serving ME/CFS patients in southwest London and Surrey.]

Abstract:
Chronic Fatigue Syndrome (CFS) is a heterogeneous disorder of unknown aetiology characterised by disabling fatigue, headaches, sleep disturbance and several other symptoms.

The onset of CFS may follow a viral infection or period of stress. Patients with CFS do not have hypogammaglobulinaemia, predisposition to recurrent bacterial infections or symptoms of autoimmunity.

To date, defects in B-cell numbers or function have not been shown in the literature. [In autoimmune disorders such as RA, immune B cells mistakenly attack self.] However, treatment with anti-B-cell therapy using Rituximab has recently shown benefit to CFS patients.

We therefore postulated that patients with CFS had a subtle humoral [found in the body fluids] immune dysfunction, and performed extended B-cell immunophenotyping.

We undertook a detailed characterization of the proportions of the different B-cell subsets in 33 patients with CFS fulfilling the Canadian and Fukuda criteria for CFS and compared these with 24 age and gender matched healthy controls (HC).

CFS patients had:

• Greater numbers of naïve B-cells as a % lymphocytes - 6.3 % versus 3.9 % in HC (P=0.034),

• Greater numbers of naïve B-cells as a % of B-cells - 65 % versus 47 % in controls (P=0.003),

• Greater numbers of transitional B-cells - 1.8 % versus 0.8 % in controls (P=0.025)

• And reduced numbers of plasmablasts - 0.5 % versus 0.9 % in controls (P=0.013).

While the cause of these changes is unclear, we speculate whether they may suggest a subtle tendency to autoimmunity.

Source: Clinical & Experimental Immunology, abstract online Nov 2012, full text article not yet formatted. DOI: 10.1111/cei.12043, by Bradley AS, Ford B, Bansal AS. Department of Immunology, St. Helier University Hospital NHS Trust, Carshalton, Surrey, UK. [Email: Amolak.Bansal@esth.nhs.uk]





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