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PLC-2 is essential for formation and maintenance of memory B cells

¹ Laboratory for Lymphocyte Differentiation and ² Laboratory for Immunological Memory, Research Center for Allergy and Immunology, RIKEN, Yokohama, Kanagawa 230-0045, Japan
³ Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka 565-0871, Japan
⁴ FIRC Institute for Molecular Oncology (IFOM), Milano, Milan 20139, Italy
⁵ Center for Blood Research Institute for Biomedical Research, Harvard Medical School, Boston, MA 02115
⁶ Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

CORRESPONDENCE Tomohiro Kurosakil: kurosaki{at}rcai.riken.jp

Resting antigen-experienced memory B cells are thought to be responsible for the more rapid and robust antibody responses after antigen reencounter, which are the hallmark of memory humoral responses. The molecular basis for the development and survival of memory B cells remains largely unknown. We report that phospholipase C (PLC) 2 is required for efficient formation of germinal center (GC) and memory B cells. Moreover, memory B cell homeostasis is severely hampered by inducible loss of PLC-2. Accordingly, mice with a conditional deletion of PLC-2 in post-GC B cells had an almost complete abrogation of the secondary antibody response. Collectively, our data suggest that PLC-2 conveys a survival signal to GC and memory B cells and that this signal is required for a productive secondary immune response.

Abbreviations used: 4OHT, 4-hydroxy tamoxifen; BAFF, B cell activating factor belonging to the TNF family; BCR, B cell receptor; CGG, chicken -globulin; cKO, conditional KO; GC, germinal center; NP, 4-hydroxy-3-nitrophenylacetyl; PLC, phospholipase C.

© 2009 Hikida et al.
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