Cited by 34Fibromyalgia and Chronic Fatigue Syndrome ResearchLong-Term Effects of COVID-19Immunodeficiency and Autoimmune Disorders

Extended B cell phenotype in patients with myalgic encephalomyelitis/chronic fatigue syndrome: a cross-sectional study

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Mensah, F, Bansal, A, Berkovitz, S, Sharma, A, Reddy, V, Leandro, M J, Cambridge, G·2016·Clinical and Experimental Immunology

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous condition of unknown aetiology characterized by multiple symptoms including fatigue, post-exertional malaise and cognitive impairment, lasting for at least 6 months. Recently, two clinical trials of B cell depletion therapy with rituximab (anti-CD20) reported convincing improvement in symptoms. A possible but undefined role for B cells has therefore been proposed. Studies of the relative percentages of B cell subsets in patients with ME/CFS have not revealed any reproducible differences from healthy controls (HC). In order to explore whether more subtle alterations in B cell subsets related to B cell differentiation exist in ME/CFS patients we used flow cytometry to immunophenotype CD19⁺ B cells. The panel utilized immunoglobulin (Ig)D, CD27 and CD38 (classical B cell subsets) together with additional markers. A total of 38 patients fulfilling Canadian, Centre for Disease Control and Fukuda ME/CFS criteria and 32 age- and sex-matched HC were included. We found no difference in percentages of classical subsets between ME/CFS patients and HC. However, we observed an increase in frequency (P < 0·01) and expression (MFI; P = 0·03) of CD24 on total B cells, confined to IgD⁺ subsets. Within memory subsets, a higher frequency of CD21⁺ CD38⁻ B cells (> 20%) was associated with the presence of ME/CFS [odds ratio: 3·47 (1·15-10·46); P = 0·03] compared with HC, and there was a negative correlation with disease duration. In conclusion, we identified possible changes in B cell phenotype in patients with ME/CFS. These may reflect altered B cell function and, if confirmed in other patient cohorts, could provide a platform for studies based on clinical course or responsiveness to rituximab therapy.

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Crossref · 10.1111/cei.12749

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Authors
Mensah, F., Bansal, A., Berkovitz, S., Sharma, A., Reddy, V, Leandro, M. J., & Cambridge, G.
Affiliations
  • University College London (GB)
  • Epsom and St Helier University Hospitals NHS Trust (GB)
  • Royal London Hospital (GB)
Corresponding author
Cambridge, G
Venue
Clinical and Experimental Immunology
Published
2016-02-22
Volume
184
Issue
2
Pages
237-247
ISSN
  • 0009-9104 (ISSN-L)
  • 1365-2249
OpenAlex
W2195523718
Cited by
34
References
75
Citations by year
2026: 1 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 4 · 2021: 4 · 2019: 4 · 2018: 5 · 2017: 4 · 2016: 3
FWCI
3.24
Type
journal article
Language
en
Open access
Locations
  • Clinical & Experimental Immunology (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Invest in ME charity (1114035)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
  • Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
Keywords
chronic fatigue syndrome, B-cell phenotype, B cell subsets, CD24, CD21, CD38, IgD, memory B cells, B cell differentiation, disease duration, rituximab, B-cell depletion therapy
MeSH terms
Rituximab, Adolescent, Adult, Aged, Cross-Sectional Studies, Female, Flow Cytometry, Humans, Immunoglobulin D, Immunologic Factors, Male, Membrane Glycoproteins, Middle Aged, Biomarkers, Fatigue Syndrome, Chronic, B-Lymphocyte Subsets, Receptors, Complement 3d, Tumor Necrosis Factor Receptor Superfamily, Member 7, Antigens, CD19, Antigens, CD20, CD24 Antigen, ADP-ribosyl Cyclase 1, Young Adult

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