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Faculty Members


Bioresponse Regulation(Biology)

Saitoh TatsuyaProfessor

I graduated from the Faculty of Pharmaceutical Sciences of Chiba University and became a pharmacist. I then entered the graduate school of Tokyo Medical and Dental University, where I obtained my Ph.D. Since becoming a researcher, I have been working on immunology. In particular, I am analyzing the regulatory mechanisms of immune responses and the relationship between immune responses and disease development. I am also working on the development of methods to control immune responses. Through research and education, I would like to contribute to the development of future pharmacist-scientists and the development of therapeutic drugs for diseases with unmet medical needs.

Research theme

Elucidation of immune responses involved in the elimination of pathogens and cancer cells

The immune system protects us by eliminating foreign substances such as pathogens and cancer cells. Our laboratory is focusing on the role of organelles such as mitochondria and intracellular degradation machineries such as autophagy to elucidate the regulatory mechanisms of immune responses induced against foreign substances.

Elucidation of the aberrant immune response that causes disease development

The immune system is often out of control and activated very strongly or unnecessarily long. Aberrant activation of the immune system damages tissues to cause allergic diseases, lifestyle-related diseases, and autoimmune diseases. Our laboratory is focusing on aberrant immune responses triggered by irritant particles and genetic mutations to elucidate the pathogenesis of immune-related diseases.

Development of therapeutic drugs based on the regulation of immune responses

Our laboratory promotes fundamental research that leads to the development of vaccines that eliminate pathogens and cancer cells, as well as new anti-inflammatory and anti-allergic drugs. We have conducted compound library screening and identified several compounds that regulate immune responses. We are working to elucidate the mechanism of action of the hit compounds and to verify their therapeutic effects using animal models.

Representative achievements

Matsui Y, Takemura N, Shirasaki Y, Takahama M, Noguchi Y, Ikoma K, Pan Y, Nishida S, Taura M, Nakayama A, Funatsu T, Misawa T, Harada Y, Sunazuka T, Saitoh T.
Nanaomycin E inhibits NLRP3 inflammasome activation by preventing mitochondrial dysfunction
Int Immunol. 2022;34(10):505-518.

Ikoma K, Takahama M, Kimishima A, Pan Y, Taura M, Nakayama A, Arai M, Takemura N, Saitoh T.
Oridonin suppresses particulate-induced NLRP3-independent IL-1α release to prevent crystallopathy in the lung
Int Immunol. 2022;34(10):493-504.

Wang J, Takemura N, Saitoh T.
Macrophage Response Driven by Extracellular ATP.
Biol Pharm Bull. 2021;44(5):599-604.

Takahama M, Akira S, Saitoh T.
Autophagy limits activation of the inflammasomes
Immunol Rev. 2018;281(1):62-73.

Takahama M, Fukuda M, Ohbayashi N, Kozaki T, Misawa T, Okamoto T, Matsuura Y, Akira S, Saitoh T.
The RAB2B-GARIL5 complex promotes cytosolic DNA-induced innate immune responses.
Cell Rep. 2017;20(12):2944-2954.

Kozaki T, Komano J, Kanbayashi D, Takahama M, Misawa T, Satoh T, Takeuchi O, Kawai T, Shimizu S, Matsuura Y, Akira S, Saitoh T.
Mitochondrial damage elicits a TCDD-inducible poly(ADP-ribose) polymerase-mediated antiviral response.
Proc Natl Acad Sci U S A. 2017;114(10):2681-2686.

Saitoh T, Akira S.
Regulation of inflammasomes by autophagy.
J Allergy Clin Immunol. 2016;138(1):28-36.

*Misawa T, *Saitoh T, Kozaki T, Park S, Takahama M, Akira S (*Contributed equally).
Resveratrol inhibits the acetylated α-tubulin-mediated assembly of the NLRP3-inflammasome.
Int Immunol. 2015;27(9):425-34.

Misawa T, Takahama M, Kozaki T, Lee H, Zou J, *Saitoh T, *Akira S.(*Corresponding authors).
Microtubule-driven spatial arrangement of mitochondria promotes activation of the NLRP3 inflammasome.
Nat Immunol. 2013;14(5):454-60.

Saitoh T, Fujita N, Jang MH, Uematsu S, Yang BG, Satoh T, Omori H, Noda T, Yamamoto N, Komatsu M, Tanaka K, Kawai T, Tsujimura T, Takeuchi O, Yoshimori T, Akira S.
Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production.
Nature. 2008;456(7219):264-8.