Pubmed-entry ::= {
  pmid 22044750,
  medent {
    em std {
      year 2012,
      month 2,
      day 6
    },
    cit {
      title {
        name "Noncollagenous 16A domain of type XVII collagen-reactive CD4+ T
 cells play a pivotal role in the development of active disease in
 experimental bullous pemphigoid model."
      },
      authors {
        names ml {
          "Ujiie H",
          "Shibaki A",
          "Nishie W",
          "Shinkuma S",
          "Moriuchi R",
          "Qiao H",
          "Shimizu H"
        },
        affil str "Department of Dermatology, Hokkaido University Graduate
 School of Medicine, Sapporo, Japan."
      },
      from journal {
        title {
          iso-jta "Clin. Immunol.",
          ml-jta "Clin Immunol",
          issn "1521-7035",
          name "Clinical immunology (Orlando, Fla.)"
        },
        imp {
          date std {
            year 2012,
            month 2
          },
          volume "142",
          issue "2",
          pages "167-175",
          language "eng",
          pubstatus ppublish,
          history {
            {
              pubstatus received,
              date std {
                year 2011,
                month 9,
                day 8
              }
            },
            {
              pubstatus revised,
              date std {
                year 2011,
                month 10,
                day 7
              }
            },
            {
              pubstatus accepted,
              date std {
                year 2011,
                month 10,
                day 7
              }
            },
            {
              pubstatus aheadofprint,
              date std {
                year 2011,
                month 10,
                day 17
              }
            },
            {
              pubstatus other,
              date std {
                year 2011,
                month 11,
                day 3,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus pubmed,
              date std {
                year 2011,
                month 11,
                day 3,
                hour 6,
                minute 0
              }
            },
            {
              pubstatus medline,
              date std {
                year 2012,
                month 4,
                day 12,
                hour 6,
                minute 0
              }
            }
          }
        }
      },
      ids {
        pii "S1521-6616(11)00301-9",
        doi "10.1016/j.clim.2011.10.002",
        pubmed 22044750
      }
    },
    abstract "Bullous pemphigoid (BP), the most common autoimmune blistering
 disease, is caused by autoantibodies against type XVII collagen (COL17). We
 recently demonstrated that CD4+ T cells were crucial for the production of
 anti-COL17 IgG and for the development of the BP phenotype by using a novel
 active BP mouse model by adoptively transferring immunized splenocytes into
 immunodeficient COL17-humanized mice. Noncollagenous 16A (NC16A) domain of
 COL17 is considered to contain the main pathogenic epitopes of BP, however,
 the pathogenicity of COL17 NC16A-reactive CD4+ T cells has never been
 elucidated. To address this issue, we modulated the immune responses against
 COL17 in active BP model by using anti-CD40 ligand (CD40L) monoclonal
 antibody MR1, an inhibitor of the CD40-CD40L interaction, in various ways.
 First, we show the essential role of CD4+ T cells in the model by showing
 that CD4+ T cells isolated from wild-type mice immunized with human COL17
 enabled naive B cells to produce anti-COL17 NC16A IgG in vivo. Second, we
 show that the activation of anti-COL17 NC16A IgG-producing B cells via
 CD40-CD40L interaction was completed within 5 days after the adoptive
 transfer of immunized splenocytes. Notably, a single administration of MR1 at
 day 0 was enough to inhibit the production of anti-COL17 NC16A IgG and to
 diminish skin lesions despite the presence of restored anti-COL17 IgG at the
 later stage. In contrast, the delayed administration of MR1 failed to inhibit
 the production of anti-COL17 NC16A IgG and the development of the BP
 phenotype. These results strongly suggest that COL17 NC16A-reactive CD4+ T
 cells play a pivotal role in the production of pathogenic autoantibodies and
 in the development of active disease in experimental BP model.",
    mesh {
      {
        term "Adoptive Transfer"
      },
      {
        term "Animals"
      },
      {
        term "Antibodies, Monoclonal",
        qual {
          {
            mp TRUE,
            subh "administration & dosage"
          },
          {
            subh "immunology"
          }
        }
      },
      {
        term "Autoantibodies",
        qual {
          {
            mp TRUE,
            subh "biosynthesis"
          },
          {
            subh "blood"
          }
        }
      },
      {
        mp TRUE,
        term "Autoantigens",
        qual {
          {
            subh "immunology"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "B-Lymphocytes",
        qual {
          {
            subh "immunology"
          },
          {
            subh "secretion"
          }
        }
      },
      {
        term "CD4-Positive T-Lymphocytes",
        qual {
          {
            mp TRUE,
            subh "immunology"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        term "CD40 Ligand",
        qual {
          {
            mp TRUE,
            subh "antagonists & inhibitors"
          },
          {
            subh "immunology"
          }
        }
      },
      {
        term "Disease Models, Animal"
      },
      {
        term "Humans"
      },
      {
        term "Immunoglobulin G",
        qual {
          {
            subh "biosynthesis"
          },
          {
            subh "blood"
          }
        }
      },
      {
        term "Mice"
      },
      {
        term "Mice, Inbred C57BL"
      },
      {
        term "Mice, Transgenic"
      },
      {
        mp TRUE,
        term "Non-Fibrillar Collagens",
        qual {
          {
            subh "immunology"
          },
          {
            subh "metabolism"
          }
        }
      },
      {
        mp TRUE,
        term "Pemphigoid, Bullous",
        qual {
          {
            subh "immunology"
          },
          {
            subh "metabolism"
          },
          {
            subh "therapy"
          }
        }
      },
      {
        term "Time Factors"
      }
    },
    substance {
      {
        type nameonly,
        name "Antibodies, Monoclonal"
      },
      {
        type nameonly,
        name "Autoantibodies"
      },
      {
        type nameonly,
        name "Autoantigens"
      },
      {
        type nameonly,
        name "Immunoglobulin G"
      },
      {
        type nameonly,
        name "Non-Fibrillar Collagens"
      },
      {
        type nameonly,
        name "collagen type XVII"
      },
      {
        type cas,
        cit "147205-72-9",
        name "CD40 Ligand"
      }
    },
    pmid 22044750,
    pub-type {
      "Journal Article",
      "Research Support, Non-U.S. Gov't"
    },
    status medline
  }
}

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