title: Screening NK-, B- and T-cell phenotype and function in patients suffering from Chronic Fatigue Syndrome.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institut de recerca de la sida, IrsiCaixa-HIVACAT, Institut d'Investigació en Ciències de la Salut Germans Trias I Pujol|, Badalona, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Curriu
authors.forename: Jorge
authors.initials: J
authors.lastname: Carrillo
authors.forename: Marta
authors.initials: M
authors.lastname: Massanella
authors.forename: Josepa
authors.initials: J
authors.lastname: Rigau
authors.forename: José
authors.initials: J
authors.lastname: Alegre
authors.forename: Jordi
authors.initials: J
authors.lastname: Puig
authors.forename: Ana M
authors.initials: AM
authors.lastname: Garcia-Quintana
authors.forename: Jesus
authors.initials: J
authors.lastname: Castro-Marrero
authors.forename: Eugènia
authors.initials: E
authors.lastname: Negredo
authors.forename: Bonaventura
authors.initials: B
authors.lastname: Clotet
authors.forename: Cecilia
authors.initials: C
authors.lastname: Cabrera
authors.forename: Julià
authors.initials: J
authors.lastname: Blanco
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology*; D016516:CD4-CD8 Ratio; D016923:Cell Death; D049109:Cell Proliferation; D016000:Cluster Analysis; D015331:Cohort Studies; D015673:Fatigue Syndrome, Chronic / Q000175:diagnosis* / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016130:Immunophenotyping; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology*; D037181:Lectins, C-Type / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D013601:T-Lymphocytes / Q000276:immunology*; D016896:Treatment Outcome; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D053645:Interleukin-2 Receptor alpha Subunit; D037181:Lectins, C-Type; D000099192:CD69 Antigens