Date:       Friday, June 12, 2015, 16:00-17:00

Venue:   2F Seminar Room,
               Center for AIDS Research, Kumamoto University

Program

16:00~16:05  Opening

Toshio Suda, Director, IRCMS

16:05~17:00 

Titile: Layered immune theory-Stem cell independent lymphopoiesis in the mouse embryo

Speaker: Momoko Yoshimoto MD., Ph.D. 

Abstract:
In developing mouse embryos, several waves of hematopoiesis occur sequentially, overlapping each other. The primitive erythropoiesis and definitive erythro-myeloid progenitors (EMPs) appear mainly in extra-embryonic yolk sac (YS), followed by the emergence of hematopoietic stem cells (HSCs) in the aorta-gonado-mesonephros (AGM) region at embryonic day (E) 11. The primitive erythropoiesis and YS EMP-derived hematopoiesis have been considered to be transient to sustain embryonic homeostasis until HSC-derived hematopoiesis is established; however, recent evidence indicates that YS EMP-derived macrophages persist as tissue macrophages in adult life. In addition, accumulated evidence indicates the presence of lymphoid cell development prior to HSC emergence, challenging the stem cell theory that all the lymphoid cells are derived from HSCs. We have demonstrated that this first wave of B lymphoid cells are derived from hemogenic endothelial cells (HECs) in both YS and para-aortic spranchnopleura (P-Sp) and belong to innate type B-1 cell lineage. These HEC-derived B-1 cells secrete natural antibodies and are transplantable when injected into the irradiated recipient peritoneal cavity: important characteristics of B-1 cells. Furthermore, in order to prove that the first wave of B cells are not HSC derived, we utilized an unique transgenic mouse model where HSC are absent in the fetal liver but EMP and few lymphoid cells exist. We have demonstrated the presence of functional transplantable B-1 progenitor cells in the HSC-deficient embryo. This proves the presence of HSC-independent lymphopoiesis and layered immune theory that was proposed by Dr. Herzenberg in1989. Our recent studies on the lineage-tracing mouse model showing HSC-independent B-1 cell contribution into post-natal life, B-1 cell self-renewal mechanisms, and application for mouse ES cell system will be described.

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