Zobrazeno 1 - 10
of 185
pro vyhledávání: '"Toshikazu Shirai"'
Autor:
Norihiro Nishimoto, Hideki Okazaki, Sachiko Hirose, Hiroyuki Nishimura, Qingshun Lin, Toshikazu Shirai, Mareki Ohtsuji, Naomi Ohtsuji, Hiromichi Tsurui, Hirofumi Amano, Keiko Nishikawa
Publikováno v:
Modern Rheumatology. 25:270-277
We earlier found that TNFα but not interleukin (IL)-17 is indispensable in the pathogenesis of spontaneously occurring rheumatoid arthritis (RA)-like disease in our newly established FcγRIIB-deficient C57BL/6 (B6) mouse model, designated KO1. Here,
Autor:
Sachiko Hirose, Toshiyuki Takai, Katsuko Sudo, Keiko Nishikawa, Masao Ono, Shozo Izui, Naomi Ohtsuji, Mareki Ohtsuji, Qingshun Lin, Rong Hou, Toshikazu Shirai, Aya Sato-Hayashizaki, Hiroyuki Nishimura, Hiromichi Tsurui
Publikováno v:
Arthritis & Rheumatism. 63:2930-2938
Objective Fcγ receptor type IIb (FcγRIIb) is a major negative regulator of B cells, and the lack of FcγRIIb expression has been reported to induce systemic lupus erythematosus (SLE) in mice of the C57BL/6 (B6) genetic background. The 129 strain–
Autor:
Aya, Sato-Hayashizaki, Mareki, Ohtsuji, Qingshun, Lin, Rong, Hou, Naomi, Ohtsuji, Keiko, Nishikawa, Hiromichi, Tsurui, Katsuko, Sudo, Masao, Ono, Shozo, Izui, Toshikazu, Shirai, Toshiyuki, Takai, Hiroyuki, Nishimura, Sachiko, Hirose
Publikováno v:
Arthritis and rheumatism
OBJECTIVE Fc? receptor type IIb (Fc?RIIb) is a major negative regulator of B cells and the lack of Fc?RIIb expression has been reported to induce systemic lupus erythematosus (SLE) in mice of the C57BL/6 (B6) genetic background. The 129 strain derive
Autor:
Yasuharu Abe, Mareki Ohtsuji, Naomi Ohtsuji, Qingshun Lin, Hiromichi Tsurui, Susumu Nakae, Toshikazu Shirai, Katsuko Sudo, Sachiko Hirose
Publikováno v:
Modern Rheumatology. 19:316-322
Autor:
Toshikazu Shirai, Katsuko Sudo, Sachiko Hirose, Kazuyuki Tsukamoto, Yi Jiang, Wakana Shiroiwa, Qingshun Lin, Hiromichi Tsurui, Kazuhiro Nakamura, Mareki Ohtsuji, Hiroyuki Nishimura
Publikováno v:
The Journal of Immunology. 180:4530-4539
Both suppressive and promoting roles of NKT cells have been reported in the pathogenesis of systemic lupus erythematosus (SLE). Herein, we found that although New Zealand mice have normal frequencies of NKT cells, their in vitro potential to produce
In a total of 283 biopsies, 100 (35%) were found to be IgA nephropathy. The incidence reached 40% among primary glomerulonephropathies. On the basis of histopathologic changes in glomeruli, these biopsies were classified into 3 groups. The criteria e
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::03d0de1c30139ea2ed7808e4ba596f1e
https://doi.org/10.1159/000401436
https://doi.org/10.1159/000401436
Autor:
Sachiko Hirose, Akinori Ida, Mareki Ohtsuji, Qingshun Lin, Toshikazu Shirai, Katsuyuki Kinoshita, Wakana Shiroiwa, Sanki Kodera, Hiromichi Tsurui, Kazuhiro Nakamura, Kazuyuki Tsukamoto, Hiroyuki Nishimura, Naomi Ohtsuji
Publikováno v:
International Immunology. 19:175-183
To thoroughly understand the role of IL-4 in the pathogenesis of systemic lupus erythematosus (SLE), a prototypic antibody-mediated systemic autoimmune disease, we examined the potential of in vitro IL-4 production by anti-CD3 mAb-stimulated splenic
Autor:
Takuma Fujii, Kenichi Ikeda, N Nishimura, Y Jikumaru, T Haga, Yuji Inada, M Yomogida, Yukiyasu Iida, Sachiko Hirose, Toshikazu Shirai, M Ninami, Yo Kodera, Hiroyuki Nishimura
Publikováno v:
Genes & Immunity. 7:647-654
The F(1) hybrid of autoimmune hemolytic anemia-prone NZB and nonautoimmune NZW strains of mice has been studied as a murine model of systemic lupus erythematosus. Both NZB and F(1) hybrid mice show age-dependent spontaneous activation of peripheral C
Publikováno v:
Springer Seminars in Immunopathology. 28:163-174
Systemic lupus erythematosus (SLE) is a systemic antibody-mediated autoimmune disease that develops under the control of multiple susceptibility genes. Genetic studies in murine and human SLE have identified several chromosomal intervals that contain
Autor:
Sachiko Hirose, Toshikazu Shirai
Publikováno v:
Springer Seminars in Immunopathology. 28:79-82