Macrophages appear to be the predominant source of IL-10 in the lungs. Human alveolar macrophages spontaneously release IL-10 and this is increased by inflammatory stimuli, such as interleukin(IL)-1P and endotoxin.7,8 Alveolar macrophages from asthmatic patients release significantly less IL-10 at baseline and in response to inflammatory stimuli than cells from normal subjects.8 A similar pattern is observed with monocytes from peripheral blood and this defect in IL-10 secretion is more marked in patients with severe compared to mild asthma, suggesting that this deficit may relate to the severity of asthma and the intensity of airway inflammation.9
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