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Regulation of Monocyte Survival In Vitro by Deposited IgG: Role of Macrophage Colony-Stimulating Factor¹

Clay B. Marsh^2,*,, Richard P. Pomerantz^*, Jennifer M. Parker^*, Alissa V. Winnard^*, Ernest L. Mazzaferri, Jr.^*, Nicanor Moldovan, Todd W. Kelley^*, Eric Beck and Mark D. Wewers^*,

^* Division of Pulmonary and Critical Care Medicine and The Heart and Lung Institute, Ohio State University College of Medicine and Public Health, Columbus, OH 43210; and Progenitor, Inc., Columbus, OH 43210

IgG deposition at tissue sites characteristically leads to macrophage accumulation and organ injury. Although the mechanism by which deposited IgG induces tissue injury is not known, we have recently demonstrated that deposited IgG stimulates the release of IL-8 and monocyte chemoattractant protein-1 from normal human monocytes, which may drive inflammation. Since IgG also induces macrophage accumulation in these diseases, we hypothesized that deposited IgG protects monocytes from apoptosis. As an in vitro model of the effect of deposited IgG on monocyte survival, monocyte apoptosis was studied after FcR cross-linking. Monocytes cultured on immobilized IgG, which induces FcR cross-linking, were protected from apoptosis, whereas monocytes cultured with equivalent concentrations of F(ab')₂ IgG or 50 times higher concentrations of soluble IgG, neither of which induces FcR cross-linking, were not protected. Moreover, this protection was transferable, as supernatants from immobilized IgG-stimulated monocytes protected freshly isolated monocytes from apoptosis and contained functional M-CSF, a known monocyte survival factor. M-CSF mediated the monocyte survival induced by FcR cross-linking, as neutralizing anti-human M-CSF Abs blocked the monocyte protection provided by either immobilized IgG or IgG-stimulated monocyte supernatants. These findings demonstrate a novel mechanism by which deposited IgG targets tissue macrophage accumulation through FcR-mediated M-CSF release. This pathway may play an important role in promoting and potentiating IgG-mediated tissue injury.

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