Screening NK-, B- and T-cell phenotype and function in patients suffering from Chronic Fatigue Syndrome

• Published in: Journal of translational medicine Vol. 11; no. 1; p. 68
• Main Authors: Curriu, Marta, Carrillo, Jorge, Massanella, Marta, Rigau, Josepa, Alegre, José, Puig, Jordi, Garcia-Quintana, Ana M, Castro-Marrero, Jesus, Negredo, Eugènia, Clotet, Bonaventura, Cabrera, Cecilia, Blanco, Julià
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 20.03.2013; BioMed Central
• Subjects: Adult; Analysis; Antigens, CD - metabolism; Antigens, Differentiation, T-Lymphocyte - metabolism; B-Lymphocytes - immunology; Care and treatment; CD4-CD8 Ratio; Cell Death; Cell Proliferation; Cells; Chronic fatigue syndrome; Cluster Analysis; Cohort Studies; Diagnosis; Fatigue Syndrome, Chronic - diagnosis; Fatigue Syndrome, Chronic - immunology; Female; Flow Cytometry; Genetic aspects; Health aspects; Humans; Immune system; Immunophenotyping; Interleukin-2 Receptor alpha Subunit - metabolism; Killer Cells, Natural - immunology; Lectins, C-Type - metabolism; Lymphocytes; Male; Memory (Computers); Middle Aged; Phenotype; T cell proliferation; T-Lymphocytes - immunology; Treatment Outcome; Viral infections; Spain
• ISSN: 1479-5876; 1479-5876
• DOI: 10.1186/1479-5876-11-68

Chronic Fatigue Syndrome (CFS) is a debilitating neuro-immune disorder of unknown etiology diagnosed by an array of clinical manifestations. Although several immunological abnormalities have been described in CFS, their heterogeneity has limited diagnostic applicability. Immunological features of CFS were screened in 22 CFS diagnosed individuals fulfilling Fukuda criteria and 30 control healthy individuals. Peripheral blood T, B and NK cell function and phenotype were analyzed by flow cytometry in both groups. CFS diagnosed individuals showed similar absolute numbers of T, B and NK cells, with minor differences in the percentage of CD4+ and CD8+ T cells. B cells showed similar subset frequencies and proliferative responses between groups. Conversely, significant differences were observed in T cell subsets. CFS individuals showed increased levels of T regulatory cells (CD25+/FOXP3+) CD4 T cells, and lower proliferative responses in vitro and in vivo. Moreover, CD8 T cells from the CFS group showed significantly lower activation and frequency of effector memory cells. No clear signs of T-cell immunosenescence were observed. NK cells from CFS individuals displayed higher expression of NKp46 and CD69 but lower expression of CD25 in all NK subsets defined. Overall, T cell and NK cell features clearly clustered CFS individuals. Our findings suggest that alterations in T-cell phenotype and proliferative response along with the specific signature of NK cell phenotype may be useful to identify CFS individuals. The striking down modulation of T cell mediated immunity may help to understand intercurrent viral infections in CFS.