Characterisation of cell functions and receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME)

Abnormal immune function is often an underlying component of illness pathophysiology and symptom presentation. Functional and phenotypic immune-related alterations may play a role in the obscure pathomechanism of Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). The objective of this study was to investigate the functional ability of innate and adaptive immune cells in moderate and severe CFS/ME patients. The 1994 Fukuda criteria for CFS/ME were used to define CFS/ME patients. CFS/ME participants were grouped based on illness severity with 15 moderately affected (moderate) and 12 severely affected (severe) CFS/ME patients who were age and sex matched with 18 healthy controls. Flow cytometric protocols were used for immunological analysis of dendritic cells, monocytes and neutrophil function as well as measures of lytic proteins and T, natural killer (NK) and B cell receptors.

CFS/ME patients exhibited alterations in NK receptors and adhesion markers and receptors on CD4⁺T and CD8⁺T cells. Moderate CFS/ME patients had increased CD8⁺ CD45RA effector memory T cells, SLAM expression on NK cells, KIR2DL5⁺ on CD4⁺T cells and BTLA4⁺ on CD4⁺T central memory cells. Moderate CFS/ME patients also had reduced CD8⁺T central memory LFA-1, total CD8⁺T KLRG1, naïve CD4⁺T KLRG1 and CD56^dimCD16⁻ NK cell CD2⁺ and CD18⁺CD2⁺. Severe CFS/ME patients had increased CD18⁺CD11c⁻ in the CD56^dimCD16⁻ NK cell phenotype and reduced NKp46 in CD56^brightCD16^dim NK cells.

This research accentuated the presence of immunological abnormalities in CFS/ME and highlighted the importance of assessing functional parameters of both innate and adaptive immune systems in the illness.