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  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0007-0963</Issn>
      <Volume>167</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Detection of antibodies against the non-calcium-dependent epitopes of desmoglein 3 in pemphigus vulgaris and their pathogenic significance</ArticleTitle>
    <FirstPage LZero="delete">252</FirstPage>
    <LastPage>261</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">K</FirstName>
        <LastName>Kamiya</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Y</FirstName>
        <LastName>Aoyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Y</FirstName>
        <LastName>Shirafuji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">T</FirstName>
        <LastName>Hamada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">S</FirstName>
        <LastName>Morizane</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">K</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">K</FirstName>
        <LastName>Hisata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">K</FirstName>
        <LastName>Iwatsuki</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background Antidesmoglein (anti-Dsg) 3 serum antibody titres are usually correlated with the disease activity of pemphigus vulgaris (PV), but some patients retain high titres even in remission. 

Objectives The aim of our study was to determine whether anti-Dsg3 antibodies in PV sera recognized calcium (Ca2+)-dependent or non-Ca2+-dependent epitopes, and to evaluate their pathogenicity. 

Methods Dsg3 baculoprotein-coated enzyme-linked immunosorbent assay (ELISA) plates were treated with 0.5 mmol L-1 ethylenediaminetetraacetic acid (EDTA). The binding ability of anti-Dsg3 monoclonal antibodies (mAbs) was analysed. Eight of the 83 patients with PV who were screened had elevated Dsg3 ELISA index values &gt; 100 in remission. The binding ability of these PV sera was analysed. We evaluated the pathogenicity of anti-Dsg3 serum antibodies against the non-Ca2+-dependent epitopes using a dissociation assay. 

Results The reactivity of pathogenic anti-Dsg3 mAbs against the Ca2+-dependent epitopes diminished markedly in the EDTA-treated ELISA, whereas no such reduction was observed in mAbs against the non-Ca2+-dependent epitopes. The sera of all the patients contained antibodies against both Ca2+-dependent and non-Ca2+-dependent epitopes. In six out of the eight patients, the ratio of antibodies against Ca2+-dependent to non-Ca2+-dependent epitopes decreased in remission. EDTA-treated Dsg3 baculoproteins adsorbed anti-Dsg3 serum antibodies against the non-Ca2+-dependent epitopes, but the remnant PV antibodies retained the ability to induce acantholysis in the dissociation assay. 

Conclusions We have established an assay to measure indirectly the titres of anti-Dsg3 serum antibodies against the Ca2+-dependent epitopes, based on the differences between EDTA-untreated and EDTA-treated ELISA index values, as a routine laboratory test to reflect the pathogenic anti-Dsg3 serum antibody titres more accurately.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>58</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2004</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections.</ArticleTitle>
    <FirstPage LZero="delete">169</FirstPage>
    <LastPage>180</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Keiji</FirstName>
        <LastName>Iwatsuki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takenobu</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuhide</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Suzuki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazuyasu</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hironori</FirstName>
        <LastName>Matsuura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Oono</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/32089</ArticleId>
    </ArticleIdList>
    <Abstract>&lt;p&gt;Epstein-Barr virus (EBV), or human herpesvirus 4 (HHV-4), infects the vast majority of adults worldwide, and establishes both nonproductive (latent) and productive (lytic) infections. Host immune responses directed against both the lytic and latent cycle-associated EBV antigens induce a diversity of clinical symptoms in patients with chronic active EBV infections who usually contain an oligoclonal pool of EBV-infected lymphocyte subsets in their blood. Episomal EBV genes in the latent infection utilize an array of evasion strategies from host immune responses: the minimized expression of EBV antigens targeted by host cytotoxic T lymphocytes (CTLs), the down-regulation of cell adhesion molecule expression, and the release of virokines to inhibit the host CTLs. The oncogenic role of latent EBV infection is not yet fully understood, but latent membrane proteins (LMPs) expressed during the latency cycle have essential biological properties leading to cellular gene expression and immortalization, and EBV-encoded gene products such as viral interleukin-10 (vIL-10) and bcl-2 homologue function to survive the EBV-infected cells. The subsequent oncogenic DNA damage may lead to the development of neoplasms. EBV-associated NK/T cell lymphoproliferative disorders are prevalent in Asia, but quite rare in Western countries. The genetic immunological background, therefore, is closely linked to the development of EBV-associated neoplasms.&lt;/p&gt;</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">latent infection</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hydroa vacciniforme</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">mosquito allergy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chronic active EB virus infection</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hemophagocytic syndrome</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName/>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn/>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2005</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The effect of formaldehyde gas exposure in a murine allergic contact hypersensitivity model</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazuyasu</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
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