Tasuku Honjo
Kyoto University
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Primary Section: 43, Immunology and Inflammation Secondary Section: 41, Medical Genetics, Hematology, and Oncology Membership Type:
International Member
(elected 2001)
Photo Credit: Kyoto University |
Biosketch
Dr. Honjo is a distinguished professor and deputy director-general at the Kyoto University Institute for Advanced Study. He recently became a director of Center for Cancer Immunotherapy and Immunobiology. He is well known for his discovery of AID that is essential for class switch recombination and somatic hypermutation. He has established the basic conceptual framework of class switch recombination. In addition, he discovered PD-1, a negative coreceptor at the effector phase of immune response and showed that PD-1 modulation contributes to treatments of tumor, viral infection and autoimmunity. For these contributions, Dr. Honjo has received many awards, including the Nobel Prize in Physiology or Medicine, JMA supreme award of merit, Imperial Prize, Japan Academy Prize, Robert Koch Prize, Order of Culture, the Tang Prize, the Kyoto Prize. Elected as a foreign associate of National Academy of Sciences, USA, as a member of the German Academy of Natural Scientists, and also as a member of Japan Academy.
Research Interests
I have studied several aspects of lymphocyte development under normal and aberrant conditions. My laboratory has demonstrated that immunoglobulin class switching is mediated by a region-specific recombination, accompanied by looping-out deletion of immunoglobulin constant-region genes from chromosomes. We have also cloned cDNA for IL-4 and IL-5 cytokines that regulate class switching. More recently we identified a putative RNA-editing enzyme, AID (activation induced cytidine deaminase), which regulates not only class switch recombination but also somatic hypermutation. This unexpected finding suggests that the two apparently different genetic alteration systems in the immunoglobulin gene locus may be regulated by yet another alteration mechanism of genetic information. Another line of studies led us to isolate the PD-1 receptor that delivers negative signaling upon interaction with its ligands PD-L1 and PD-L2. PD-1 deficiency causes autoimmune symptoms such as systemic lupus erythematosus in C57/BL mice and dilated cardiomyopathy in BALB/c mice, indicating that PD-1 plays important roles in immune tolerance. We have identified the suppressor of Hairless gene in Drosophila and its mammalian homologue RBP-J, which has been shown to be the direct signaling target of the Notch receptor and to regulate lineage commitment and differentiation of varieties of cells, including lymphocytes.
