スポンサーリンク
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo | 論文
- The Role of IFN-γ and Toll-Like Receptors in Nephropathy Induced by Toxoplasma gondii Infection
- Evaluation of the Effects of Sulfamethoxazole on Toxoplasma gondii Loads and Stage Conversion in IFN-γ Knockout Mice Using QC-PCR
- Pathogenicity of Toxoplasma gondii through B-2 Cell-Mediated Downregulation of Host Defense Responses
- CD44 and Bak Expression in IL-6 or TNF-alpha Gene Knockout Mice After Whole Lung Irradiation
- Interleukin-1β and macrophage migration inhibitory factor (MIF) in dermal fibroblasts mediate UVA-induced matrix metalloproteinase-1 expression
- IL-1α, but not IL-1β, is required for contact-allergen-specific T cell activation during the sensitization phase in contact hypersensitivity
- Dectin-1 Is Not Required for the Host Defense to Cryptococcus neoformans
- Involvement of IL-17 in Fas ligand-induced inflammation
- Different Mutation Frequencies and Spectra among Organs by N-Melthyl-N-nitrosourea in rpsL (strA) Transgenic Mice
- Differential roles for IFN-γ and IL-17 in experimental autoimmune uveoretinitis
- Interleukin 1 Receptor Antagonist Is Important in the Suppression of Neointima Formation after Injury
- 3P-220 Tet-OFF遺伝子発現システムを用いた小脳学習におけるMAPK/ERK kinase1の機能解析(生体膜/人工膜・情報伝達,第46回日本生物物理学会年会)
- Diurnal Variation of Heart Rate, Locomotor Activity, and Body Temperature in Interleukin-1α/β Doubly Deficient Mice
- OE-363 Deficiency of Interleukin-1 Receptor Antagonist Induces Aortic Valve Stenosis in BALB/c Mice(Valvular heart disease/Pericarditis/Cardiac tumor-1, The 71st Annual Scientific Meeting of the Japanese Circulation Society)
- Presence of A Higher Molecular Weight β-1, 4-Galactosyltransferase in Mouse Liver
- Role of Tumor Necrosis Factor-Alpha and Interferon-Gamma in Helicobacter pylori Infection
- IL-1β, but not IL-1α, is required for antigen-specific T cell activation and the induction of local inflammation in the delayed-type hypersensitivity responses
- Abnormal T cell activation caused by the imbalance of the IL-1/IL-1R antagonist system is responsible for the development of experimental autoimmune encephalomyelitis
- IL-1 is required for allergen-specific T_h2 cell activation and the development of airway hypersensitivity response
- IL-1-induced tumor necrosis factor-α elicits inflammatory cell infiltration in the skin by inducing IFN-γ-inducible protein 10 in the elicitation phase of the contact hypersensitivity response