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2 Is Essential for Specific Functions of Fc
R and FcR1
* The Blood Research Institute, The Blood Center of Southeastern Wisconsin, Milwaukee, WI 53226;
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan;
Institute of Molecular Medicine, Nanjing University, Nanjing, Peoples Republic of China;
Department of Pharmacology, Byk Gulden, Konstanz, Germany; and
¶ Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI 53226
Phospholipase C
2 (PLC2) plays a critical role in the
functions of the B cell receptor in B cells and of the FcR
chain-containing collagen receptor in platelets. Here we report that
PLC2 is also expressed in mast cells and monocytes/macrophages and
is activated by cross-linking of Fc
R and FcR. Although
PLC2-deficient mice have normal development and numbers of mast
cells and monocytes/macrophages, we demonstrate that PLC2 is
essential for specific functions of FcR and FcR. While
PLC2-deficient mast cells have normal mitogen-activated protein
kinase activation and cytokine production at mRNA levels, the mutant
cells have impaired FcR-mediated Ca2+ flux and inositol
1,4,5-trisphosphate production, degranulation, and cytokine secretion.
As a physiological consequence of the effect of PLC2 deficiency, the
mutant mice are resistant to IgE-mediated cutaneous inflammatory skin
reaction. Macrophages from PLC2-deficient mice have no detectable
FcR-mediated Ca2+ flux; however, the mutant cells have
normal FcR-mediated phagocytosis. Moreover, PLC2 plays a
nonredundant role in FcR-mediated inflammatory skin
reaction.
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