Related Experiment Video
Updated: May 8, 2025
Human In Vitro Suppression as Screening Tool for the Recognition of an Early State of Immune Imbalance
Published on: July 22, 2011
Reduction of non-classical monocytes that suppress interferon-α in patients with systemic lupus erythematosus
Akina Ishii1, Shingo Nakayamada2, Naoaki Ohkubo2
1The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu; and Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
Objectives:
Monocytes are known to be involved in both adaptive and innate immune responses, though their roles in the pathogenesis of systemic lupus erythematosus (SLE) are still unclear. Here, we performed phenotypic and functional analyses of each monocyte subset.
Methods:
Peripheral blood from patients with autoimmune diseases (SLE: n=53, rheumatoid arthritis: n=12, systemic sclerosis: n=36) was analysed using flow cytometry to compare the number of each monocyte subset and the expression levels of the cell surface markers of patients to those of healthy donors (n=28).
Results:
The number of CD14dimCD16+ non-classical monocytes in peripheral blood from SLE patients was significantly decreased compared with those from healthy donors and patients with other autoimmune diseases. The number of circulating non-classical monocytes was inversely correlated to SLE disease activity. The number of non-classical monocytes was not related to the use of glucocorticoids or to the presence or absence of specific tissue inflammation. The expression levels of cell surface molecules and the survival rate of non-classical monocytes of patients with SLE were similar to those of healthy donors. An in vitro functional assay revealed that non-classical monocytes suppressed IFN-α production from PBMCs or plasmacytoid DCs, and cell-cell contact through ICAM-4 seemed to be important in this process.
Conclusions:
Our study demonstrated that the number of circulating non-classical monocytes, which has been shown to have the ability to suppress IFN-α production, was decreased in SLE patients, and this might be related to the excess IFN signature in SLE patients.
