Professor: Shinsuke TAKI
Associate Professor: Takuma HAYASHI
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One of the pillars of the research in our laboratory is to clarify the regulatory mechanisms of the immune system and to address how the failure of such mechanisms results in immune-based diseases such as autoimmune diseases and allergy. As another pillar, a project is also underway to unveil the relationship between defective proteasome pathway and spontaneous development of diseases, specifically tumor progression and optic neuropaty. To achieve these goals, we mainly take approaches in which a battery of gene-manipulated animals as well as materials from human patients.The specific current research interests are as follows: |
*Regulatory mechanism for the differentiation of the helper T cell subsets Th1 and Th2
*Pathogenic mechanism of dermal inflammation spontaneously developing due to the aberration of type I interferon signaling
*Transcriptional regulation of NK and NKT cell differentiation
*Molecular basis for uterine leiomyosarcoma tumorigenesis, involing defective LMP2 expression
*Mechanism for the optic neuropathy normal tension glaucoma, caused by impaired NFkB fucntions |
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- Hida,S.,et al. Fc receptor Α-chain, a constitutive component of the IL-3 receptor, is required for IL-3-induced IL-4 production in basophils. Nature Immunol. 10:214-222, 2009.
- Nakajima,S.,et al. IL-15 inhibits pre-B cell proliferation by selectively expanding Mac-1+B220+ NK cells. Biochem. Biophys. Res. Commun. 369:1139-1143, 2008.
- Arakura,F.,et al. Genetic control directed towards spontaneous IFN-Ώ/ΐ responses and downstream IFN-Α expression influences the pathogenesis of a murine psoriasis-like skin disease. J. Immunol. 179 (17):3249-3257, 2007.
- Takahashi,Y.,et al. Development of spontaneous optic neuropathy in NF-ΘBp50-deficient mice;Requirement for NF-ΘBp50 in ganglion cell survival. Neuropathol. Appl. Neurobiol. 33(6):692-705, 2007.
- Hayashi,T.,et al. The mutation in the ATP-binding region of JAK1, identified in human uterine leiomyosarcomas, results in defective interferon- inducibility of TAP1 and LMP2. Oncogene 25(29):4016-26, 2006.
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