Essential role for ICSBP in the in vivo development of murine CD8α+ dendritic cells

DOI PDF 被引用文献17件
  • Julio Aliberti
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Oliver Schulz
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Daniel J. Pennington
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Hideki Tsujimura
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Caetano Reis e Sousa
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Keiko Ozato
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.
  • Alan Sher
    From the Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), and Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte Molecular Biology Laboratories, Cancer Research United Kingdom, London Research Institute, London, United Kingdom.

抄録

<jats:title>Abstract</jats:title><jats:p>Interferon (IFN) consensus sequence-binding protein (ICSBP) is an important transcription factor regulating proinflammatory cytokine production and the development of mononuclear phagocytes in vitro. Here we analyzed the role of ICSBP in the in vivo differentiation of 3 major subsets of murine dendritic cells (DCs). We found that ICSBP is predominantly expressed by the CD8α+ subset, and more important, that ICSBP−/− mice have a profound and selective deficiency in CD8α+ DEC205+ DCs in lymphoid tissues. Studies using wild-type/ICSBP−/−chimeras revealed that this defect in CD8α+ DC development is intrinsic to bone marrow–derived progenitors and not dependent on ICSBP expression in the nonhemopoietic compartment. Because DC precursor frequencies are unaltered in the bone marrow of ICSBP−/− mice, ICSBP appears to function by regulating CD8α+ DC differentiation downstream from the generation of common DC progenitors. Although CD8α− DCs are present in normal numbers in ICSBP−/− animals, up-regulation of CD40, CD80, and major histocompatibility complex (MHC) class II expression was found to be impaired in this subset after in vivo microbial stimulation. Together these results demonstrate that ICSBP is critically required for the in vivo differentiation of CD8α+ DCs and may also influence the functional maturation of the CD8α− subsets.</jats:p>

収録刊行物

  • Blood

    Blood 101 (1), 305-310, 2003-01-01

    American Society of Hematology

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