title: Increased expression of CD16, CD69, and very late antigen-1 on blood monocytes in active sarcoidosis.
abstract: BACKGROUND
  Different types of immune cells are involved in the formation of granulomas, a hallmark of pulmonary sarcoidosis. Proinflammatory monocytes are activated circulating monocytes thought to be related to the initial events of granuloma formation. We tested the hypothesis that peripheral blood monocytes in patients with active pulmonary sarcoidosis have an activated phenotype and, secondly, that measuring this activation status can provide a new tool for monitoring disease activity.
  
  
  METHODS
  Blood was collected of 23 steroid-naive patients presenting with pulmonary sarcoidosis and 10 healthy control subjects. Expression of CD16 (Fc-gamma type III receptor), CD69 (a general activation marker of cells of the hematopoietic lineage), and the integrin very late antigen (VLA)-1 (on interaction with extracellular matrix compounds mediates cell adhesion) was measured by flow cytometry.
  
  
  RESULTS
  Percentages of monocytes expressing CD16, CD69, and VLA-1 in patients vs control subjects were 56.2 +/- 4.1% vs 12.2 +/- 2.4% (p < 0.0001), 87.3 +/- 2.1% vs 8.6 +/- 3.3% (p < 0.0001), and 66.5 +/- 3.6% vs 11.2 +/- 2.3% (p < 0.0001), respectively. Moreover, the CD69+VLA-1+ monocyte subset, abundantly present at disease presentation, was found to decrease to normal levels during follow-up with disease remission.
  
  
  CONCLUSIONS
  Peripheral blood monocytes from patients with pulmonary sarcoidosis show a highly activated phenotype. Phenotyping circulating monocytes might be a promising tool for monitoring sarcoidosis disease activity but needs further investigation.
authors.affiliation: Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
authors.forename: Michiel
authors.initials: M
authors.lastname: Heron
authors.affiliation: Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands. Electronic address: j.grutters@antonius.net.
authors.forename: Jan C
authors.initials: JC
authors.lastname: Grutters
authors.affiliation: Department of Medical Microbiology and Immunology, St. Antonius Hospital, Nieuwegein, the Netherlands.
authors.forename: Heleen
authors.initials: H
authors.lastname: van Velzen-Blad
authors.affiliation: Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
authors.forename: Marcel
authors.initials: M
authors.lastname: Veltkamp
authors.affiliation: Department of Medical Microbiology and Immunology, St. Antonius Hospital, Nieuwegein, the Netherlands.
authors.forename: Anke M E
authors.initials: AME
authors.lastname: Claessen
authors.affiliation: Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
authors.forename: Jules M M
authors.initials: JMM
authors.lastname: van den Bosch
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000096:biosynthesis*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis*; D015415:Biomarkers / Q000097:blood; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology; D016130:Immunophenotyping; D039222:Integrin alpha1beta1 / Q000096:biosynthesis*; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology / Q000378:metabolism*; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D017452:Receptors, IgG / Q000096:biosynthesis*; D017565:Sarcoidosis, Pulmonary / Q000097:blood* / Q000276:immunology; D012720:Severity of Illness Index; D055815:Young Adult; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D015415:Biomarkers; D039222:Integrin alpha1beta1; D037181:Lectins, C-Type; D007703:Peptidyl-Dipeptidase A; D017452:Receptors, IgG; D000099192:CD69 Antigens