Infection and Prevention

kaoOsamu Takeuchi Professor   btn

The innate immune system directly recognizes infection of pathogens including viruses and bacteria via microbial sensors such as Toll-like receptors (TLRs). The TLR signaling results in the production of cytokines and evokes inflammation. We are studying the molecular mechanisms of inflammation caused by innate immunity by using model mice. We are focusing on 1) Regulation of cytokine production by RNA stability control. 2) Mechanisms of TLR signaling. 3)Transcriptional control in response to TLR stimulation.

Research and Education

Viral and bacterial infection is initially recognized by the host innate immune system. Pattern recognition receptors such as Toll-like receptors (TLRs) initiate intracellular signaling pathways leading to the production of cytokines and causing inflammation (Fig. 1). Inflammation is related not only to infectious diseases, but also to various common diseases including autoimmune disease, cancer and metabolic disorders. We are studying molecular mechanisms of inflammation from innate immunity point of view. Particularly we are focusing on transcriptional and posttranscriptional regulation of genes relating to inflammation. We discovered an RNase, named Regnase-1, which is responsible for destabilizing cytokine mRNAs and prevention of inflammatory diseases. We will study how the balance is taken between transcription and degradation (Takeuchi, Mino). We are also studying on inflammation and redox regulation (Masutani).
Graduate students in our lab will learn skills on molecular biology and immunology. We welcome young students who are interested in our research.

スライド1Regulation of innate immune responses


Laboratory members

Recent Publications

  1. Tartey, S., Matsushita, K., Imamura, T., Wakabayashi, A., Ori, D., Mino, T., Takeuchi, O. (2015). Essential Function for the Nuclear Protein Akirin2 in B Cell Activation and Humoral Immune Responses. J. Immunol. 195, 519-527.
  2. Mino, T., Murakawa, Y., Fukao, A., Vandenbon, A., Wessels, H.-H., Ori, D., Uehata, T., Tartey, S., Akira, S., Suzuki, Y., Vinuesa, C.G., Ohler, U., Standley,D.M., Landthaler, M., Fujiwara, T., Takeuchi, O. (2015). Regnase-1 and Roquin Regulate a Common Element in Inflammatory mRNAs by Spatiotemporally Distinct Mechanisms. Cell 161, 1058–
  3. Tartey, S., Matsushita, K., Vandenbon, A., Ori, D., Imamura, T., Mino, T., Standley, D.M., Hoffmann, J.A., Reichhart, J.M., Akira, S., Takeuchi, O. (2014). Akirin2 is critical for inducing inflammatory genes by bridging IκB-ζ and the SWI/SNF complex. EMBO J. 33, 2332-2348.
  4. Uehata, T., Iwasaki, H., Vandenbon, Matsushita, K., Cuellar, E.H., Kuniyoshi, K., Satoh, T., Mino, T., Suzuki, Y., Standley, D.M., Tsujimura, T., Rakugi, H., Isaka, Y., Takeuchi, O., Akira, S. (2013). Malt1-Induced Cleavage of Regnase-1 in CD4+ Helper T Cells Regulates Immune Activation. Cell 153, 1036-1049.
  5. *Matsushita, K., *Takeuchi, O., Standley, D.M., Kumagai, Y., Kawagoe, T., Miyake, T., Satoh, T., Kato, H., Tsujimura, T., Nakamura, H., Akira, S. (*Equal contribution). (2009). Zc3h12a is an RNase essential for controlling immune responses by regulating mRNA decay. Nature 458, 1185-1190.


Professor: Osamu Takeuchi
Associate Professor: Hiroshi Masutani
Assistant Professor: Takashi Mino