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Effects of Cytapheresis on Tumor Necrosis Factor Receptor and on Expression of CD63 in Myeloperoxidase–Antineutrophil Cytoplasmic Autoantibody‐associated Vasculitis
Author(s) -
Hasegawa Midori,
Nishii Chikako,
Kabutan Nao,
Kato Masao,
Ohashi Atsushi,
Nakai Shigeru,
Murakami Kazutaka,
Tomita Makoto,
Nabeshima Kunihiro,
Hiki Yoshiyuki,
Oshima Hisaji,
Sugiyama Satoshi
Publication year - 2007
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1744-9987.2007.00496.x
Subject(s) - medicine , myeloperoxidase , cd63 , autoantibody , vasculitis , tumor necrosis factor alpha , immunology , inflammation , antibody , disease , biochemistry , microrna , chemistry , microvesicles , gene
To evaluate the therapeutic potential of cytapheresis in myeloperoxidase–antineutrophil cytoplasmic autoantibody (MPO–ANCA)‐associated vasculitis, plasma levels of soluble tumor necrosis factor receptors (sTNFR1, sTNFR2) and the expression of TNFR1, TNFR2, and CD63 on granulocytes were measured. The levels of sTNFR1 and sTNFR2, and the expression of TNFR1 and TNFR2 were significantly higher in MPO–ANCA‐associated vasculitis patients than in normal controls. The levels of sTNFR1 and sTNFR2 increased significantly after cytapheresis ( P < 0.001). The expression of TNFR1 showed a tendency to decrease after cytapheresis ( P = 0.0535). The expression of CD63 decreased significantly after cytapheresis ( P < 0.05). Because sTNFR1 and sTNFR2 act as TNF‐antagonists, the increases of sTNFR1 and sTNFR2 after cytapheresis might contribute to inhibit the action of TNF‐α. The decreased expression of TNFR1, which mediates the signal for polymorphonuclear cell respiratory burst, might also contribute to the reduction of inflammation. From these results, the inhibition of TNF action and removal of degranulated granulocytes appear to be related to the mechanism whereby cytapheresis can exert a beneficial and therapeutic function in the treatment of MPO–ANCA‐associated vasculitis.