A photo of Koichi Araki.

Koichi Araki, DVM, PhD


  • Division of Infectious Diseases
  • Assistant Professor, UC Department of Pediatrics

About

Biography

I received my PhD from Hokkaido University, Japan. During my PhD study, I became interested in infectious diseases and T cell immunity.

In my laboratory, I’ve studied CD8 T cell immunity, which is important for controlling viral infections and intracellular bacterial and parasitic infections. It is now clear that CD8 T cells are also involved in immunity against tumors. There is considerable interest in cancer immunotherapy that stimulates CD8 T cell immunity.

My research focus is to understand the mechanisms of how antigen specific CD8 T cell responses are regulated during acute and chronic infection. I’m looking into investigating the role of 1) translational regulation, 2) mTOR activity, and 3) autophagy in effector, memory and exhausted T cell differentiation. The ultimate goal of my research is to develop novel drugs or strategies from information obtained in my basic studies to cure diseases by modulating the immune system.

My studies of CD8 T cell immunity can help us learn and develop better methods to prevent and treat infectious diseases. It also has applications in immunotherapy for cancer treatment against tumors.

I have been a researcher for more than a decade and began my work at Cincinnati Children’s in 2019.

DVM: School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan, 2000.

PhD: School of Veterinary Medicine, Hokkaido University, Hokkaido, Japan, 2004.

Postdoctoral Fellow: Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, 2011.

Research Areas

Infectious Diseases, Inflammation and Tolerance, Immunobiology

Publications

Mitochondrial metabolic flexibility is critical for CD8+ T cell antitumor immunity. Chen, C; Zheng, H; Horwitz, EM; Ando, S; Araki, K; Zhao, P; Li, Z; Ford, ML; Ahmed, R; Qu, C. Science Advances. 2023; 9:eadf9522.

PD-1 blockade increases the self-renewal of stem-like CD8 T cells to compensate for their accelerated differentiation into effectors. Gill, AL; Wang, PH; Lee, J; Hudson, WH; Ando, S; Araki, K; Hu, Y; Wieland, A; Im, S; Gavora, A; Medina, CB; Freeman, GJ; Hashimoto, M; Reiner, SL; Ahmed, R. Science Immunology. 2023; 8:eadg0539.

mTOR regulates T cell exhaustion and PD-1-targeted immunotherapy response during chronic viral infection. Ando, S; Perkins, CM; Sajiki, Y; Chastain, C; Valanparambil, RM; Wieland, A; Hudson, WH; Hashimoto, M; Ramalingam, SS; Freeman, GJ; Ahmed, R; Araki, K. The Journal of Clinical Investigation. 2023; 133:e160025.

CD8 T-cell heterogeneity during T-cell exhaustion and PD-1-targeted immunotherapy. Ando, S; Araki, K. International Immunology. 2022; 34:571-577.

PD-1 combination therapy with IL-2 modifies CD8+ T cell exhaustion program. Hashimoto, M; Araki, K; Cardenas, MA; Li, P; Jadhav, RR; Kissick, HT; Hudson, WH; McGuire, DJ; Obeng, RC; Wieland, A; Umaña, P; Leonard, WJ; Smith, KA; Ahmed, R. Nature. 2022; 610:173-181.

CD45RB Status of CD8+ T Cell Memory Defines T Cell Receptor Affinity and Persistence. Krummey, SM; Morris, AB; Jacobs, JR; McGuire, DJ; Ando, S; Tong, KP; Zhang, W; Robertson, J; Guasch, SA; Araki, K; Larsen, CP; Evavold, BD; Kissick, HT; Ford, ML. Cell Reports. 2020; 30:1282-1291.e5.