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The Journal of Immunology, Vol 157, Issue 8 3220-3222, Copyright © 1996 by American Association of Immunologists

CUTTING EDGE

Impaired IL-13-mediated functions of macrophages in STAT6-deficient mice

K Takeda, M Kamanaka, T Tanaka, T Kishimoto and S Akira
Institute for Molecular and Cellular Biology, Osaka University, Japan.

IL-13 shares many biologic responses with IL-4. In contrast to well- characterized IL-4 signaling pathways, which utilize STAT6 and 4PS/IRS2, IL-13 signaling pathways are poorly understood. Recent studies performed with STAT6-deficient mice have demonstrated that STAT6 plays an essential role in IL-4 signaling. In this study, the functions of peritoneal macrophages of STAT6-deficient mice in response to IL-13 were analyzed. In STAT6-deficient mice, neither morphologic changes nor augmentation of MHC class II expression in response to IL- 13 was observed. In addition, IL-13 did not decrease the nitric oxide production by activated macrophages. Taken together, these results suggest that the macrophage functions in response to IL-13 were impaired in STAT6-deficient mice, indicating that IL-13 and IL-4 share the signaling pathway via STAT6.


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