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The Journal of Immunology, 2003, 170: 6355-6362.
Copyright © 2003 by The American Association of Immunologists

Failure of Monocytes of Trauma Patients to Convert to Immature Dendritic Cells is Related to Preferential Macrophage-Colony-Stimulating Factor-Driven Macrophage Differentiation1

Asit K. De2,*, Krzysztof Laudanski2,* and Carol L. Miller-Graziano3,*,{dagger}

Departments of * Surgery and {dagger} Microbiology/Immunology, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642

Following trauma, increased inflammatory monokine activation and depressed APC function can occur simultaneously. These contradictory monocyte (M{phi}) dysfunctions could result if postinjury M{phi} differentiation preferentially favored inflammatory macrophage (Mac) differentiation over development into the most potent APC, dendritic cells (DC). In this report, M{phi} of trauma patients with a depressed MLR induction capacity are, for the first time, shown to be unable to differentiate in vitro to immature CD1a+ DC under the influence of GM-CSF and IL-4. Trauma patient M{phi} that retained MLR-inducing capacity had a nonsignificant reduction in DC differentiation capacity. Only patient M{phi} populations with depressed differentiation to immature DC (iDC) demonstrated depressed IL-12 and IL-15 production and a continued reduced MLR induction capacity. Neither increased IL-10 production nor decreased CD11c+ DC precursor numbers correlated with depressed M{phi}-to-DC differentiation. Instead, these patients’ APC-dysfunctional M{phi} populations had increased expression of inflammatory Mac phenotypes (CD64+, CD86low, HLA-DRlow) and up-regulated secretion of M-CSF. M-CSF combined with IL-6 inhibits M{phi}-to-iDC differentiation and promotes M{phi}-to-Mac differentiation by down-regulating GM-CSFR expression and increasing DC apoptosis. Both depressed GM-CSFR expression and increased M{phi} iDC apoptosis, as well as increased expression of CD126 (IL-6R) and CD115 (M-CSFR), were detected in APC-defective patient M{phi}. In vitro addition of anti-M-CSF enhanced the IL-4 plus GM-CSF-induced M{phi}-to-DC differentiation of these patients. This suggests that, in trauma patients, enhanced M{phi}-to-Mac differentiation with concomitant inhibited iDC development is partially due to increased circulating M{phi} sensitivity to and production of M-CSF and contributes to postinjury immunoaberrations.




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