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(Journal of Leukocyte Biology. 2001;70:624-632.)
© 2001 by Society for Leukocyte Biology

IL-10 receptor dysfunction in macrophages during chronic inflammation

Rita Avdiushko, David Hongo, Helene Lake-Bullock, Alan Kaplan and Donald Cohen

Department of Microbiology and Immunology, University of Kentucky, College of Medicine, Lexington

Correspondence: Dr. Donald Cohen, Department of Microbiology and Immunology, University of Kentucky, College of Medicine, 800 Rose St., Lexington, KY 40536-0084. E-mail: dcohen{at}pop.uky.edu

The immunosuppressive activity of interleukin-10 (IL-10) makes this cytokine a potentially important clinical tool to reduce inflammatory responses in various diseases. Its efficacy as a therapeutic modality is dependent on the responsiveness of immune cells. We report that macrophages from mice chronically infected with the LP-BM5 retrovirus had a reduced capacity to respond to IL-10 in vitro. The ability of IL-10 to inhibit lipopolysaccharide-induced production of tumor necrosis factor (TNF) {alpha} and IL-6 was significantly reduced in both alveolar and peritoneal macrophages from infected versus uninfected mice. IL-10 hyporesponsiveness was not related to direct infection by the retrovirus, because bone marrow-derived macrophages infected in vitro with LP-BM5 were as responsive to IL-10 as were uninfected bone marrow-derived macrophages. TNF-{alpha} appeared to contribute to development of IL-10 hyporesponsiveness, because exposure of normal macrophages to TNF-{alpha} but not interferon-{gamma} reduced macrophage responsiveness to IL-10. Reverse transcriptase-PCR and flow cytometry demonstrated normal expression of the {alpha} and ß chains of the IL-10 receptor in macrophages from infected mice, suggesting that IL-10 hyporesponsiveness is not related to a change in receptor expression. The potential role of reduced IL-10 responsiveness in the chronicity of inflammation in this and other diseases is discussed.

Key Words: cytokine • inflammation • retroviruses • TNF-{alpha}




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