Impaired IL-13-mediated functions of macrophages in STAT6-deficient mice.
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.
Takeda
K
K
Institute for Molecular and Cellular Biology, Osaka University, Japan.
Kamanaka
M
M
Tanaka
T
T
Kishimoto
T
T
Akira
S
S
D000818:Animals; D001483:Base Sequence; D017931:DNA Primers / Q000235:genetics; D015870:Gene Expression; D000949:Histocompatibility Antigens Class II / Q000235:genetics; D018793:Interleukin-13 / Q000494:pharmacology* / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000276:immunology* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D050800:STAT6 Transcription Factor; D015398:Signal Transduction; D015534:Trans-Activators / Q000172:deficiency* / Q000235:genetics / Q000276:immunology
D017931:DNA Primers; D000949:Histocompatibility Antigens Class II; D018793:Interleukin-13; D050800:STAT6 Transcription Factor; C494100:Stat6 protein, mouse; D015534:Trans-Activators; D015847:Interleukin-4; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase