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KMID : 0357119930150020163
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Korean Journal of Immunology
1993 Volume.15 No. 2 p.163 ~ p.171
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Regulation Mechanisms of Inflammatory Response Induced by FcrR Stimulation in Human Monocytes and Monocytic Cell Line, THP1
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Yoon Kang-Soon
Yoon Suk-Ran
Lee Choong-Eu
Kim Hyung-Soo
Pyun Kwang-Ho
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Abstract
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Regulation mechanisms of inflammatory responses induced by FcrR stimulation in human monocytes and monocytic cell line THP1 were investigated. Release of arachidonic acid, which is the precusor for inflammatory mediators, was induced by FcrR stimulation with its ligand human IgG or with anti FcrR mAbs. This response was further increased when FcrR was cross-linked with in-soluble anti-IgG-agarose and soluble anti-IgG Fc specific Fab fragments. These phenomena were shown in both monocyte and THP1. Oxidative burst activity, resulting from generation of reactive oxygen speices, was also induced by FcrR stimulation and further enhanced by cross-linking of Fcr R. Induction mechanisms of inflammatory responses caused by PMA or FcrR stimulations were then examined by measurements of release of arachidonic acid and oxidative burst activity. The results demonstrate that monocytes utilize different signaling pathways for FcrR or PMA stimulation. Signaling mechanism of PMA stimulation is especially dependent on Ca}+/calmodulin dependent kinase in arachidonic acid release, but not in oxidative burst activity. Meanwhile, signaling pathways of FcrR are dependent on tyrosine kinase but independent of protein kinase C both in the release of arachidonic acid and oxidative burst activity. The results suggest that in monocytes, there is a not only functional but also mechanistic link between arachidonic acid release and oxidative burst activity induced upon FcrR stimulation. Distinct signaling pathways seem to be operating in transformed monocytic cell line THP-1 cells, and no mechanistic link was found between arachidonic acid release and oxidative burst activity induced after FcrR stimulation.
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KEYWORD
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FcrR, Inflammatory Response, Arachidonic Acid Release, Oxidative Burst Activity, Signaling Pathways
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