Increased expression of CD16, CD69, and very late antigen-1 on blood monocytes in active sarcoidosis.
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.
Heron
Michiel
M
Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
Grutters
Jan C
JC
Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands. Electronic address: j.grutters@antonius.net.
van Velzen-Blad
Heleen
H
Department of Medical Microbiology and Immunology, St. Antonius Hospital, Nieuwegein, the Netherlands.
Veltkamp
Marcel
M
Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
Claessen
Anke M E
AME
Department of Medical Microbiology and Immunology, St. Antonius Hospital, Nieuwegein, the Netherlands.
van den Bosch
Jules M M
JMM
Center for Interstitial Lung Diseases, Department of Pulmonology, St. Antonius Hospital, Nieuwegein, the Netherlands.
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
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