Asian Pac J Allergy Immunol. 2016 Mar 20. doi: 10.12932/AP0733. [Epub ahead of print]
Regulatory T, natural killer T and γδ T cells in multiple sclerosis and chronic fatigue syndrome/myalgic encephalomyelitis: a comparison.
Ramos S1, Brenu E, Broadley S, Kwiatek R, Ng J, Nguyen T, Freeman S, Staines D, Marshall-Gradisnik S.
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 (γδ T) cells may also be dysregulated in CFS/ME and MS.
To evaluate and compare specific immune regulatory cells of patients with CFS/ME, patients with MS and healthy controls.
Sixty three volunteers were included in this study, 24 were CFS/ME patients, 11 MS patients and 27 healthy controls. Blood samples were obtained from all the participants for flow cytometer analysis of iNKT cell, Tregs and γδ T cell phenotypes.
We observed significant increase in Tregs in the CFS/ME group (p≤0.005) compared with the healthy controls group. Total γδ and γδ 2 T cells were significantly reduced in the MS patients in comparison with the healthy controls group. Conversely, CD4+iNKT percentage of iNKT, was significantly increased in the CFS/ME group compared with healthy controls and double negative iNKT percentage of iNKT significantly decreased compared with the healthy controls group.
This study has not identified immunological disturbances that are common in both MS and CFS/ME patients. However differential expression of cell types between the conditions investigated suggests different pathways of disease. These differences need to be explored in further studies.
Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease.
Sakaguchi S, et al. Immunol Rev. 2006.
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Naturally arising CD25+ CD4+ regulatory T (Treg) cells, most of which are produced by the normal thymus as a functionally mature T-cell subpopulation, play key roles in the maintenance of immunologic self-tolerance and negative control of a variety of physiological and pathological immune responses. Natural Tregs specifically express Foxp3, a transcription factor that plays a critical role in their development and function. Complete depletion of Foxp3-expressing natural Tregs, whether they are CD25+ or CD25-, activates even weak or rare self-reactive T-cell clones, inducing severe and widespread autoimmune/inflammatory diseases. Natural Tregs are highly dependent on exogenously provided interleukin (IL)-2 for their survival in the periphery. In addition to Foxp3 and IL-2/IL-2 receptor, deficiency or functional alteration of other molecules, expressed by T cells or non-T cells, may affect the development/function of Tregs or self-reactive T cells, or both, and consequently tip the peripheral balance between the two populations toward autoimmunity. Elucidation of the molecular and cellular basis of this Treg-mediated active maintenance of self-tolerance will facilitate both our understanding of the pathogenetic mechanism of autoimmune disease and the development of novel methods of autoimmune disease prevention and treatment via enhancing and re-establishing Treg-mediated dominant control over self-reactive T cells.
And now, a translation.... someone? Anyone? Please? I don't speak immunology beyond the very basics.