寄生虫感染症学

概要

本講座では移植?AIDSの患者に見られる日和見感染症の免疫学的解析を中心に188bet体育_188bet备用网址を行っています。免疫学?感染症学を習得し、幅広い分野で活躍する人材を育成します。(画像はニューモシスチス肺炎の原因であるPneumocystisのシスト)

Research task in our Department is to clarify the mechanism of immune responses to opportunistic infection in patients with AIDS and transplant recipients.

188bet体育_188bet备用网址テーマ

  1. リコンビナント抗肺炎球菌ヒト抗体による肺炎球菌感染症の治療
    Treatment of streptococcosis with recombinant human IgG against Streptococcus pneumoniae
    (Kazunaga AGEMATSU)
  2. 細胞内寄生原虫トキソプラズマ感染に対する宿主防御応答の解析
    Study on host defense against intracellular protozoan parasite, Toxoplasma gondii
    (Fumie AOSAI, Masaya TAKAMOTO)
  3. カリニ肺炎の制御に関する分子群の免疫学的解析
    Study on molecules regulating Pneunocystis pneumonia
    (Masaya TAKAMOTO)
  4. リーシュマニア感染に対する防御機構の解明
    Study on defensive mechanisms of Leishmania infection
    (Hisashi NAGASE)

スタッフ

教授

高本 雅哉(兼務?特任)

188bet体育_188bet备用网址室の所在及び連絡先

旭総合188bet体育_188bet备用网址棟6階
0263-37-2625
e-mail: masayat(アドレスには @shinshu-u.ac.jpを付けて下さい)

主要な成果/Major Publications

  1. Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome.
    Minegishi Y, Saito M, Nagasawa M, Takada H, Hara T, Tsuchiya S, Agematsu K, Yamada M, Kawamura N, Ariga T, Tsuge I, Karasuyama H.
    J Exp Med. 206(6):1291-301, 2009.
  2. Interleukin-1beta suppression in Blau syndrome: comment on the article by Martin et al.
    Masumoto J, Yamazaki T, Ohta K, Nakayama J, Agematsu K.
    Arthritis Rheum. 60(8):2544-5, 2009.
  3. Fc receptor γ-chain, a constitutive component of the IL-3 receptor, is required for IL-3-induced IL-4 production in basophils. Hida S, Yamasaki S, Sakamoto Y, Takamoto M, Obata K, Takai T, Karasuyama H, Sugane K, Saito T, Taki S: Nat Immunol 2009 Feb;10(2):214-22.
  4. Exposure to Bisphenol A Prenatally or in Adulthood Promotes TH2 Cytokine Production Associated with Reduction of CD4+CD25+ Regulatory T Cells.Yan H, Takamoto M, Sugane K. Environ Health Perspect. 2008 Apr;116(4):514-9.
  5. Despite increased CD4+Foxp3+ cells within the infection site, BALB/c IL-4 receptor-deficient mice reveal CD4+Foxp3-negative T cells as a source of IL-10 in Leishmania major susceptibility.
    Nagase H, Jones KM, Anderson CF, Noben-Trauth N.
    J Immunol. 179(4):2435-44, 2007.

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