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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3855-3863
Mast Cells Induce Autoantibody-Mediated Vasculitis Syndrome Through
Tumor Necrosis Factor Production Upon Triggering Fc Receptors
Norihiko Watanabe,
Bunshiro Akikusa,
Seung Yong Park,
Hiroshi Ohno,
Liliane Fossati,
Gianluca Vecchietti,
J. Engelbert Gessner,
Reinhold E. Schmidt,
J. Sjef Verbeek,
Bernhard Ryffel,
Itsuo Iwamoto,
Shozo Izui, and
Takashi Saito
From the Department of Molecular Genetics, Graduate School of
Medicine, the Second Department of Pathology, School of Medicine, and
the Second Department of Internal Medicine, Chiba University, Chiba,
Japan; the Department of Pathology, Centre Medical Universitaire,
University of Geneva, Geneva, Switzerland; the Department of Clinical
Immunology, Hannover Medical School, Hannover, Germany; the Department
of Human and Clinical Genetics, Leiden University Medical Center,
Leiden, The Netherlands; and the Department of Immunology, University
of Cape Town, Groote Schuur Hospital, Observatory, South Africa.
The generation of autoantibodies and deposition of immune complexes
(ICs) in tissue play a primary role in autoimmune diseases. However,
the IC-triggered response consists of complex mechanisms that make it
difficult to identify the pathogenesis and develop specific therapy. We
clarified here a sequential mechanism for the induction of
hypersensitivity angiitis by analyzing the responsible Fc receptor
(FcR), effector cells, and mediators in an animal model using
FcR-deficient mice. In this model, rheumatoid factor-mediated skin
vasculitis was induced in wild-type mice, whereas FcR -deficient mice
did not develop the vasculitis. Adoptive transfer of various FcR+ cells into FcR-deficient mice showed that mast
cells but not macrophages derived from wild-type mice triggered skin
vasculitis. Mast cells derived from either FcRIII-deficient or tumor
necrosis factor (TNF)-deficient mice did not possess the inducibility
of skin vasculitis. These results indicate that triggering of vascular inflammation was induced by mast cells through IC binding on FcRIII. TNF produced by such activated mast cells was mainly responsible for
the pathogenesis of autoantibody-mediated vasculitis. These findings
illustrate the clinical significance of mast cells, Fc receptors,
and TNF in IC-induced vasculitis syndrome.
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