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Monocytes cultured in cytokine‐defined environments differ from freshly isolated monocytes in their responses to IL‐4 and IL‐10

To investigate the regulatory effects of the prototypic Th2 lymphocyte products and potential immunotherapeutic agents interleukin‐4 (IL‐4) and IL‐10 on macrophages differentiated in vitro under different cytokine‐defined environments, blood monocytes were incubated for 7 days in the presence of granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), macrophage colony‐stimulating factor or IL‐4. The effect of monocyte culture in the presence or absence of serum was also investigated. Functional responses by 7‐day‐cultured cells to IL‐4, quantified as decreased CD 14 expression and suppression of lipopolysaccharide (LPS)‐induced tumor necrosis factor‐α (TNF‐α) and IL‐1β production, and as a positive response, increased CD23 expression, were compared directly with the responses by monocytes from which they were derived. In response to IL‐10, decreases in LPS‐induced TNF‐α and IL‐lβ production and reduction in the expression of major histocompatibility complex (MHC) class II antigens were examined. Seven‐day cultured monocytes/macrophages showed (1) diminished TNF‐α production in response to IL‐10 but not EL‐4 (2), diminished IL‐1β production in response to both IL‐4 and IL‐10, and compared with fresh monocytes (3), diminished CD14 expression in response to IL‐4, and (4) a lesser increase in CD23 expression in response to IL‐4. This was the case regardless of the cytokine in the presence of which the cells had been cultured for 7 days. Monocytes cultured for 7 days in GM‐CSF expressed increased levels of MHC class II and LPS‐induced TNF‐α and responded inefficiently to IL‐10 for decreased MHC class II. The responses by monocytes cultured for 7 days with GM‐CSF resemble the published properties of synovial fluid macrophages from patients with chronic inflammatory arthritis. The study highlights the complexity of monocyte/macrophage responses to the immunoregulatory cytokines IL‐4 and IL‐10 and concludes that responses to IL‐4 and IL‐10 by blood monocytes may not be representative of responses by their differentiated or activated counterparts. J. Leukoc. Biol. 57: 909–918; 1995.