Drug-induced neutropenia associated with anti-neutrophil cytoplasmic antibodies (ANCA): possible involvement of complement in granulocyte cytotoxicity

Author:

Akamizu T1,Ozaki S1,Hiratani H1,Uesugi H1,Sobajima J1,Hataya Y1,Kanamoto N1,Saijo M1,Hattori Y1,Moriyama K1,Ohmori K2,Nakao K1

Affiliation:

1. Department of Medicine and Clinical Science and

2. Department of Laboratory Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan

Abstract

Summary Although antineutrophil antibodies are thought to be involved in drug-induced neutropenia, neither the precise mechanisms nor the particular antigens on the neutrophil surface have yet been clarified. Recently, we examined a patient with Graves’ disease who developed antineutrophil cytoplasmic antibodies (ANCA) after propylthiouracil treatment and exhibited neutropenia. Because several target antigens of ANCA are expressed on the surface of neutrophils, it was suggested that ANCA might contribute to neutropenia. The patient’s serum bound specifically to neutrophils and HL-60 cells differentiated into granulocytes, and lysed the HL-60 cells via a complement-mediated mechanism. Furthermore, two representative ANCA antigens, proteinase 3 and myeloperoxidase, significantly inhibited both the binding and cytotoxicity of the serum. Finally, tumour necrosis factor-α, which is known to up-regulate cell surface expression of several ANCA antigens, enhanced both the binding and cytotoxicity of the serum. These findings suggest that ANCA induced by propylthiouracil contributed to leucopenia through a complement-mediated mechanism.

Publisher

Oxford University Press (OUP)

Subject

Immunology,Immunology and Allergy

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