Kyushu University Academic Staff Educational and Research Activities Database
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Daiji Sakata Last modified date:2019.06.25





E-Mail
Phone
092-642-6830
Fax
092-642-6829
Academic Degree
PhD
Country of degree conferring institution (Overseas)
No
Field of Specialization
Immunology, Pharmacology, neuroimmunology
Total Priod of education and research career in the foreign country
03years00months
Research
Research Interests
  • Analysis of roles of DOCK family and related molecules in neuroimmune system
    keyword : immune system, inflammation, neuroimmune system
    2016.04~2021.03.
Academic Activities
Papers
1. Ushijima M., Uruno T., Nishikimi A., Sanematsu F., Kamikaseda Y., Kunimura K., Sakata D., Okada T., Fukui Y., The Rac Activator DOCK2 Mediates Plasma Cell Differentiation and IgG Antibody Production., Front. Immunol., 9:243, (2018), 1-14, 2018.02, A hallmark of humoral immune responses is the production of antibodies. This process involves a complex cascade of molecular and cellular interactions, including recognition of specific antigen by the B cell receptor (BCR), which triggers activation of B cells and differentiation into plasma cells (PCs). Although activation of the small GTPase Rac has been implicated in BCR-mediated antigen recognition, its precise role in humoral immunity and the upstream regulator remain elusive. DOCK2 is a Rac-specific guanine nucleotide exchange factor predominantly expressed in hematopoietic cells. We found that BCR-mediated Rac activation was almost completely lost in DOCK2-deficient B cells, resulting in defects in B cell spreading over the target cell-membrane and sustained growth of BCR microclusters at the interface. When wild-type B cells were stimulated in vitro with anti-IgM F(ab')2 antibody in the presence of IL-4 and IL-5, they differentiated efficiently into PCs. However, BCR-mediated PC differentiation was severely impaired in the case of DOCK2-deficient B cells. Similar results were obtained in vivo when DOCK2-deficient B cells expressing a defined BCR specificity were adoptively transferred into mice and challenged with the cognate antigen. In addition, by generating the conditional knockout mice, we found that DOCK2 expression in B-cell lineage is required to mount antigen-specific IgG antibody. These results highlight important role of the DOCK2-Rac axis in PC differentiation and IgG antibody responses..