Appearance of increased proportions of monocytes bearing the 72kd(FcRI) receptor for IgG correlated to aberrant monocyte (Mø) functions, depressed immune functions, and poor clinical outcome. The trauma patients' FeRI+ Mø subpopulation produced the majority of their elevated IL-6, TNFα, TGFβ and PGE2, IgG stimulation of patients' Mø through FeRI not only stimulated TNFα, IL-6, and PGE2 levels, but also greatly augmented the levls of these monokines produced after subsequent bacterial challenge. Post-trauma increased IL-6 levels can lead to polyclonal E-cell activation and high levels of circulating, nonspecific IgG as seen in trauma patients. This nonspecific IgG triggers the FeRI on the increased numbers of FeRI+ Mø leading to ever-increasing monokine levels. IL-4 was found to downregulate patients' FeRI+ Mø production of mediators. The cycle of altered cytokine levels, increased FeRI+ Mø numbers, elevated IgG, and augmented triggering of FeRI+ Mø may be broken by addition of IL-4.
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