Sie sind hier: FRIAS School of Life Sciences … Fellows Tomohiro Kurosaki

Tomohiro Kurosaki

External Senior Fellow
June 2010 - October 2012

1.WPI Immunology Frontier Research Center, Osaka University and
2.RIKEN Research Center for Allergy and Immunology, Yokohama, Japan

Tel. 81-45-503-7019
Fax 81-45-503-7018



Tomohiro Kurosaki was born in Okayama, Japan, in 1955. He received his M.D. in 1980 from Okayama University Medical School and his Ph.D. in 1987 from Kyoto University. After he obtained his Ph.D., he did his postdoctoral fellowship at the Sloan-Kettering Institute in New York. He then joined Lederle Laboratories till 1996 as a senior research scientist, while holding the position of adjunct assistant professor in Yale University in the United States. After returning to Japan, he directed and taught at the Institute for Liver Research at Kansai Medical University. He joined RIKEN in 2001 and has been a group director of his own research group since 2004. Also, he joined Osaka University in 2008 and has been a specially appointed professor in WPI Immunology Frontier Research Center (IFReC). His current research fields include signal transduction mechanisms through BCR and elucidation of how memory B cells are generated.

FRIAS Project

Molecular basis underlying longevity of naive B cells and memory B cells

The cellular outcomes of B cell receptor (BCR) signaling events, for example, proliferation, differentiation, or survival, are dependent on the developmental stage of the B cells and the quality/quantity of these signals. Our laboratory has focused on understanding the molecular mechanisms of signaling pathways that lead to maintain naïve and memory B cells.

During my sabbatical stay in Freiburg, I would like to exchange ideas and set up possible collaborations with the FRIAS school and the LIFNET of FRIAS; particularly with Michael Reth’s, Wolfgang Schamel’s, and Ralf Baumeister’s teams.

1) How does BCR transmit a signal? It is known that the BCR on the surface of resting naïve B cells transmits a low level constitutive signal in a ligand-independent manner (called “tonic signal”). These results were obtained with naïve B cells. We have recently obtained the data allowing us to propose that antigen-experienced memory B cells utilize a similar mechanism for their maintenance. Hence, by exchanging our on-going data with those of the Reth’s and Schamel’s groups, I will be in a position to design key experiments for testing our model (tonic signals in the case of memory B cells).

2) What is the molecular basis underlying the longevity of antigen-experienced memory B cells? Since one of the important unique properties of memory B cells is their ability to survive longer than naïve cells, Baumeister’s study can give us lots of important clues. Indeed, similar to Baumeister’s group data, we already showed the importance of PI3K activity in naive B cell maintenance. In addition, we already initiated experiments to address the importance of PI3K activity in memory B cell maintenance. By exchanging our recent data, I would like to discuss with Baumeister the nature of longevity in both BCR and IIS signaling contexts.

3) In addition I am looking forward to exchange with my German colleagues the current strategies of the promotion of science in Japan and the role that science plays for the advances of the Japanese society.


Selected Publications

  1. R. Ouchida H. Mori K. Hase H. Takatsu, T. Kurosaki, T. Tokuhisa H. Ohno J.Y. Wang: Critical role of the IgM Fc receptor in IgM homeostasis, B-cell survival, and humoral immune responses. P Natl Acad Sci Usa, 2012.