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* Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555;
Department of General Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan; and
Shriners Hospital for Children, Galveston, TX 77555
Classically activated macrophages (CAM
) have been described as a major effector cell on the host’s innate immunities. However, CAM are not generated in immunocompromised hosts whose alternatively activated macrophages (AAM) predominate. In this study, the mechanism by which AAM suppress the ability of resident macrophages (RM) to generate CAM was investigated. AAM were isolated from peritoneal exudates of mice 2 days after third-degree thermal injuries affecting 15% total body surface area. CAM were generated from RM (peritoneal M from normal mice) through stimulation with CpG DNA, a typical CAM inducer. RM did not polarize to CAM when they were cultured with AAM in a dual-chamber Transwell even when supplemented with CpG DNA. In addition, RM stimulated with CpG DNA did not convert to CAM when they were cultured with the culture fluids of AAM (AAM Culture-Sup). AAM Culture-Sup contained IL-6, IL-10, CCL17, PGE2, and TGF-
. Among these, CCL17 and IL-10 inhibited CAM generation. The ability of AAM Culture-Sup to inhibit CAM generation was eliminated when the Culture-Sup was treated with a mixture of mAbs directed against CCL17 and IL-10. These results indicate that CCL17 and IL-10 released from AAM inhibit CAM generation from RM stimulated with CpG DNA.
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