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Articles by R Nakamura
Total Records ( 2 ) for R Nakamura
  W Zhou , J Longmate , S. F Lacey , J. M Palmer , G Gallez Hawkins , L Thao , R Spielberger , R Nakamura , S. J Forman , J. A Zaia and D. J. Diamond
 

Reconstitution of cytomegalovirus (CMV)–specific CD8+ T cells is essential to the control of CMV infection in CMV-positive recipients (R+) after allogeneic hematopoietic stem cell transplantation (HCT). Six-color flow cytometry was used to assess the functional profile of CMV-specific CD8+ T cells in 62 of 178 R+ HCT recipients followed virologically for CMV reactivation. R+ recipients receiving grafts from CMV-negative donors (D; D/R+) reconstituted fewer multifunctional CD8+ T cells expressing tumor necrosis factor- (TNF-), macrophage inflammatory protein-1β (MIP-1β), and CD107 in addition to interferon- (IFN-), compared with D+/R+ recipients. Unlike monofunctional CD8+ T cells secreting IFN-, which were abundantly generated during CMV reactivation in D/R+ recipients, the relative lack of multifunctional CD8+ T cells persisted until at least 1 year post-HCT. D/R+ recipients were more likely to require recurrent and prolonged use of antivirals. These findings were robust to statistical adjustment for pretransplant factors, as well as for posttransplant factors including graft-versus-host disease (GVHD) and its treatment by steroids. These analyses suggest that D+/R+ transplants, on average, generate higher levels of multifunctional CMV-specific T cells and require less antiviral therapy compared with D/R+ HCT recipients. These results highlight the benefit of D+ donors in improving outcomes of R+ HCT recipients by reducing the duration and recurrent need of antiviral treatment, aided by increased levels of multifunctional CMV-specific T cells.

  K Gotoh , Y Tanaka , A Nishikimi , R Nakamura , H Yamada , N Maeda , T Ishikawa , K Hoshino , T Uruno , Q Cao , S Higashi , Y Kawaguchi , M Enjoji , R Takayanagi , T Kaisho , Y Yoshikai and Y. Fukui
 

Plasmacytoid dendritic cells (pDCs) play a key role in antiviral immunity, but also contribute to the pathogenesis of certain autoimmune diseases, by producing large amounts of type I IFNs. Although activation of pDCs is triggered by engagement of nucleotide-sensing toll-like receptors (TLR) 7 and 9, type I IFN induction additionally requires IB kinase (IKK) –dependent activation of IFN regulatory factor (IRF) 7. However, the signaling pathway mediating IKK- activation is poorly defined. We show that DOCK2, an atypical Rac activator, is essential for TLR7- and TLR9-mediated IFN- induction in pDCs. We found that the exposure of pDCs to nucleic acid ligands induces Rac activation through a TLR-independent and DOCK2-dependent mechanism. Although this Rac activation was dispensable for induction of inflammatory cytokines, phosphorylation of IKK- and nuclear translocation of IRF-7 were impaired in Dock2-deficient pDCs, resulting in selective loss of IFN- induction. Similar results were obtained when a dominant-negative Rac mutant was expressed in wild-type pDCs. Thus, the DOCK2–Rac signaling pathway acts in parallel with TLR engagement to control IKK- activation for type I IFN induction. Owing to its hematopoietic cell-specific expression, DOCK2 may serve as a therapeutic target for type I IFN–related autoimmune diseases.

 
 
 
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