title: Effects of cytapheresis on tumor necrosis factor receptor and on expression of CD63 in myeloperoxidase--antineutrophil cytoplasmic autoantibody-associated vasculitis.
abstract: 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-alpha. 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.
authors.affiliation: Department of Nephrology, Fujita Health University School of Medicine, Toyoake, Aichi, Japan. mhase@fujita-hu.ac.jp
authors.forename: Midori
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Chikako
authors.initials: C
authors.lastname: Nishii
authors.forename: Nao
authors.initials: N
authors.lastname: Kabutan
authors.forename: Masao
authors.initials: M
authors.lastname: Kato
authors.forename: Atsushi
authors.initials: A
authors.lastname: Ohashi
authors.forename: Shigeru
authors.initials: S
authors.lastname: Nakai
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Murakami
authors.forename: Makoto
authors.initials: M
authors.lastname: Tomita
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Nabeshima
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Hiki
authors.forename: Hisaji
authors.initials: H
authors.lastname: Oshima
authors.forename: Satoshi
authors.initials: S
authors.lastname: Sugiyama
mesh_terms: D000368:Aged; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000276:immunology*; D015703:Antigens, CD / Q000097:blood*; D016238:Cytapheresis; D005260:Female; D006098:Granulocytes / Q000737:chemistry; D006801:Humans; D008297:Male; D008875:Middle Aged; D009195:Peroxidase / Q000276:immunology*; D010980:Platelet Membrane Glycoproteins; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood*; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood*; D060149:Tetraspanin 30; D014657:Vasculitis / Q000276:immunology / Q000628:therapy*
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic; D015703:Antigens, CD; C554586:CD63 protein, human; D010980:Platelet Membrane Glycoproteins; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D060149:Tetraspanin 30; D009195:Peroxidase