第 1258 回 MYC関連転写因子によるリンパ球増殖とガン抑制プログラム演者： 栄川 健 教授 (ワシントン大学医学部 Department of Pathology and Immunology, Washington University School of Medicine )
場所： 京都大学ウイルス再生研２号館（旧ウイルス研本館）１階 セミナー室
Clonal expansion of antigen-specific T and B lymphocytes, which are present only at low frequency under steady state conditions, is a hallmark feature of adaptive immunity. They are the most rapidly dividing cells postnatally. Robust clonal expansion of T cells is directly relevant to the quantitative magnitude of immune responses and is required for eradication of rapidly replicating intracellular pathogens as well as the establishment of immunological memory. B cells also undergo continued rapid clonal expansion in the germinal centers to diversify their antibody repertoire by AID-dependent somatic hypermutation, which will be subjected to affinity-based selection. Clonal expansion of T and B cells in immune responses and of their precursors during the development is required for protective immunity. However, it is a highly metabolically demanding process and is believed to be tumor-prone due the presence of DNA damage due to AID- or RAG dependent DNA editing. Given that incidence of tumors derived from lymphocytes, such as acute lymphoblastic lymphoma or non-Hodgkin lymphoma, is relatively low compared to carcinomas, such as breast cancers and colon cancers, we hypothesize that lymphocytes have evolved to efficiently achieve robust proliferation and simultaneously protect them from transformation during immune responses. However, it remains unknown how they balance these contradictory demands to protect host from invading pathogens and oncogenic transformation. I will discuss our published and unpublished findings that provide insights into the mechanisms by which this protective mechanism is regulat-ed by a single cascade of transcriptional regulators.
Chou C et al., Immunity. 2016 Sep 20;45(3):570-82. PubMed PMID: 27566940
Chou C et al., Nat Immunol. 2014 Sep;15(9):884-93. PubMed PMID: 25029552
連絡先：ウイルス感染研究部門感染防御分野 竹内 理 （TEL：751−4024）