| Secretariat, Alumni Association, IDAC | |
| Date | Monday, 9 December 2024, 16:00～ |
|---|---|
| Room | 7th floor, Seminar Room (1), IDAC Center for Aging Research |
| Title | Lymphocyte Proliferation and Differentiation, Insights into Lymphomagenesis and T Cell Exhaustion |
| Speaker | Takeshi Egawa, MD, PhD (Professor of Pathology and Immunology) |
| Affiliation | Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, USA |
| Organizer | Yasuhisa Matsui (Cell Resource Center for Biomedical Research, ext.8571) Akiko Satoh (Department of Integrative Physiology, ext.8544) |
| Abstract | Lymphocytes are capable of robust expansion upon antigen receptor stimulation and are one of the most rapidly dividing cells in postnatal organisms. Such robust proliferative capacity is critical for establishing broad antigen receptor repertoires during development and for quantitatively amplifying antigen-specific immunity upon pathogen invasion. However, like many other primary cells, they have limited proliferative capacity as expanding lymphocytes undergo terminal differentiation with transient functionality at the expense of their longevity. Such transition of an undifferentiated progenitor cell to more mature states following a proliferative burst is seen at several checkpoints during the development of lymphocytes as well as other cell types. We predict that such cell differentiation or loss of the progenitor states is a process controlled by gene regulatory circuitry closely associated with rapid cell proliferation although the molecular basis remains undefined. Furthermore, the maintenance of population dynamics rather than the size of each population, by generating newly differentiated cells, may be fundamental for sustaining functionality of a specific cell population. We have been studying the biological significance of the tight coupling of the restriction of cell stemness with cell proliferation, potential manipulation to overcome the restriction, and consequences of perturbed population turnover in lymphocytes. I will discuss these questions in the context of gene regulatory networks initiated by the transcription factor c-MYC, tumor suppression and T cell exhaustion.
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