4.3 Article

Regulatory T, natural killer T and γδ T cells in multiple sclerosis and chronic fatigue syndrome/myalgic encephalomyelitis: a comparison

Journal

ASIAN PACIFIC JOURNAL OF ALLERGY AND IMMUNOLOGY
Volume 34, Issue 4, Pages 300-305

Publisher

ALLERGY IMMUNOL SOC THAILAND,
DOI: 10.12932/AP0733

Keywords

Chronic Fatigue Syndrome; Myalgic Encephalomyelitis; Multiple Sclerosis; Regulatory T cells, natural killer T cells; gamma delta T cells

Funding

  1. Alison Hunter Memorial Foundation
  2. Mason Foundation [MA43120]
  3. Queensland Government Department of Science, Information Technology, and Innovation & the Arts Smart Futures Fund [216702MRE]

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Background: Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME), and Multiple Sclerosis (MS) may share some similarities in relation to reduced NK cell activity. It is likely that other cells such as regulatory T (Tregs), invariant Natural Killer T (iNKT) and gamma delta T (gamma delta T) cells may also be dysregulated in CFS/ME and MS. Objective: To evaluate and compare specific immune regulatory cells of patients with CFS/ME, patients with MS and healthy controls. Method: Sixty three volunteers were included in this study: 24 were CFS/ME patients, 11 were MS patients and 27 were: healthy controls. Blood samples were obtained from all participant's for flow cytometry analysis of iNKT cells, Tregs and gamma delta T cell phenotypes. Results: We observed a significant increase in Tregs in the CFS/ME group.(p <= 0.05) compared to the healthy control group. Total gamma delta and gamma delta 2 T cells were significantly reduced in MS patients in comparison with the healthy control group. Conversely, CD4(+)iNKT percentage of iNkT, was Significantly increased in the CFS/ME group compared with healthy controls and the double-negative iNKT percentage of iNKT significantly decreased compared with the healthy control group. Conclusions: This study has not identified any immunological disturbances that are common in both MS and CFS/ME patients. However, the differential expression of cell types between the conditions investigated suggests different pathways of disease. These differences need to be explored in further studies.

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