Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
J Immunol. 1994 Oct 15;153(8):3734-44.

Lipopolysaccharide-dependent induction of IL-10 receptor expression on murine fibroblasts.

Author information

  • 1Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110.


Although various biologic activities of IL-10 have been identified, little is known about IL-10's molecular mechanism of action. Herein we report the characterization of IL-10R on different murine cell lines and demonstrate the LPS inducibility of this protein. With the use of purified recombinant murine IL-10 and labeled IL-10-specific mAb, IL-10Rs were detected by flow cytometry. Radioligand binding analyses showed that RAW264.7 cells expressed 238 +/- 87 receptors per cell and bound ligand with a single affinity of 8.3 +/- 2.4 x 10(9) M-1. Similar studies documented IL-10R expression on murine B cells (CH27) and CD4+ Th1 cells but not murine Th2 cells, L929 or WA-17 fibroblasts, or fibrosarcoma cells. Exposure of fibroblasts to LPS-induced cellular IL-10 binding activity in a dose- and time-dependent manner. Radioligand binding analyses performed on LPS-treated fibroblasts showed cellular expression of 325 +/- 59 IL-10 binding sites and a binding affinity of Ka = 7.5 +/- 2.5 x 10(8) M-1. RT-PCR analysis confirmed the induction of the IL-10R. Functional analyses of IL-10R-expressing cells revealed that IL-10 activated a cellular transcription factor in RAW264.7 cells that bound a DNA probe containing the IFN-gamma response region from the Fc gamma RI gene. In contrast, IL-10 did not induce gamma response region binding activity in L929 fibroblasts either treated with LPS or transfected with the murine IL-10R cDNA. These results thus indicate that cellular responses to IL-10 may be influenced by both the external environment and the presence of additional signaling components within the cell.

[PubMed - indexed for MEDLINE]

LinkOut - more resources

Full Text Sources

Other Literature Sources

PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Write to the Help Desk