Co-Investigator(Kenkyū-buntansha) |
IWABUCHI Kazuya Hokkaido University, Inst. Gene. Med., Asso. Prof, 遺伝子病制御研究所, 助教授 (20184898)
YANAGAWA Yoshiki Hokkaido University, Inst Gene. Med., Lec., 遺伝子病制御研究所, 助手 (20322852)
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Budget Amount *help |
¥111,410,000 (Direct Cost: ¥85,700,000、Indirect Cost: ¥25,710,000)
Fiscal Year 2006: ¥11,700,000 (Direct Cost: ¥9,000,000、Indirect Cost: ¥2,700,000)
Fiscal Year 2005: ¥13,260,000 (Direct Cost: ¥10,200,000、Indirect Cost: ¥3,060,000)
Fiscal Year 2004: ¥14,560,000 (Direct Cost: ¥11,200,000、Indirect Cost: ¥3,360,000)
Fiscal Year 2003: ¥23,530,000 (Direct Cost: ¥18,100,000、Indirect Cost: ¥5,430,000)
Fiscal Year 2002: ¥48,360,000 (Direct Cost: ¥37,200,000、Indirect Cost: ¥11,160,000)
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Research Abstract |
A new NK-T deficient strain of mice, SL/Kh, was found, where differentiation of NK-T cells was arrested at the CD40^<high> NK1.1-Ly49C/I-stage. Chemokine induced not only chemotaxis but also various functions, i.e. antigen uptake, in dendritic cells (DC), which present lipid antigens to NK-T cells (Blood 2002; 2003; Int. Immunol. 2005). DC functions to modulate Th differentiation were analyzed under different conditions (Immunology 2003a, b, c). It was found that different signal transduction systems were involved in the different cytokine productions in DC (Immunology 2006; J. Immunol. in press). Negative feed back regulation via cytokine was discovered between DC and NK-T cell interaction (Blood 2005). NK-T cells aggravated hepatitis by producing osteopontin (Immunity 2004). The osteopontin was also involved in aggravation of uveoretinitis model (J. Immunol. in press). In an arthritis model, however, NK-T cells ameliorated the clinical manifestation (Int. J. Mol. Med. 2006). Abnormal function of NK-T cells was observed in patients with Wegener's granulomatosis (Clin. Exp. Immunol. 2004). NK-T cells aggravated the atherosclerosis by producing IFN-y upon stimulation with oxidized low density lipoprotein (LDL) in murine atherosclerosis model.
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