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Monocytes migrate through the blood to the peripheral tissues, where they can develop into dendritic cells (DC) and macrophages.Studies on the phenotype of peripheral blood monocytes in rheumatic diseases revealed changes in the number of CD16+ monocytes and in the adhesive, chemotactic, antigen presenting and inflammatory properties of the cells.However, these studies often resulted in fragmented and inconsistent data and are hampered by the heterogeneity and overlap of the rheumatic diseases.By microarray analysis, changes in gene expression-profiles are detectable and subsequent correlation of the data reveals functional pathways forming a "gene expression signature".Determination of monocyte gene expression signatures in patient groups with rheumatic diseases has resulted in the detection of an Interferon (IFN) Type I induced signature in subgroups of patients with rheumatoid arthritis, Sjögren's Syndrome, systemic sclerosis and systemic lupus erythematosus.We assume that such profiling, which is robust, will lead to the development of better classification criteria and an insight into at least one functional pathogenic pathway leading to disease, i.e. the one mediated by IFN type 1.
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Brkić et al. (2010) studied this question.
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