start-ver=1.4 cd-journal=joma no-vol=167 cd-vols= no-issue=2 article-no= start-page=252 end-page=261 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201208 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Detection of antibodies against the non-calcium-dependent epitopes of desmoglein 3 in pemphigus vulgaris and their pathogenic significance en-subtitle= kn-subtitle= en-abstract= kn-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 > 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. en-copyright= kn-copyright= en-aut-name=KamiyaK en-aut-sei=Kamiya en-aut-mei=K kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=AoyamaY en-aut-sei=Aoyama en-aut-mei=Y kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=ShirafujiY en-aut-sei=Shirafuji en-aut-mei=Y kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HamadaT en-aut-sei=Hamada en-aut-mei=T kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MorizaneS en-aut-sei=Morizane en-aut-mei=S kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=FujiiK en-aut-sei=Fujii en-aut-mei=K kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HisataK en-aut-sei=Hisata en-aut-mei=K kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=IwatsukiK en-aut-sei=Iwatsuki en-aut-mei=K kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci affil-num=8 en-affil= kn-affil=Okayama Univ, Dept Dermatol, Grad Sch Med Dent & Pharmaceut Sci END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=4 article-no= start-page=169 end-page=180 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=A spectrum of clinical manifestations caused by host immune responses against Epstein-Barr virus infections. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=IwatsukiKeiji en-aut-sei=Iwatsuki en-aut-mei=Keiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YamamotoTakenobu en-aut-sei=Yamamoto en-aut-mei=Takenobu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TsujiKazuhide en-aut-sei=Tsuji en-aut-mei=Kazuhide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=SuzukiDaisuke en-aut-sei=Suzuki en-aut-mei=Daisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujiiKazuyasu en-aut-sei=Fujii en-aut-mei=Kazuyasu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsuuraHironori en-aut-sei=Matsuura en-aut-mei=Hironori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=OonoTakashi en-aut-sei=Oono en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University en-keyword=latent infection kn-keyword=latent infection en-keyword=hydroa vacciniforme kn-keyword=hydroa vacciniforme en-keyword=mosquito allergy kn-keyword=mosquito allergy en-keyword=chronic active EB virus infection kn-keyword=chronic active EB virus infection en-keyword=hemophagocytic syndrome kn-keyword=hemophagocytic syndrome END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050325 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=マウスアレルギー性接触過敏反応におけるホルムアルデヒドガスの曝露の影響 kn-title=The effect of formaldehyde gas exposure in a murine allergic contact hypersensitivity model en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=FujiiKazuyasu en-aut-sei=Fujii en-aut-mei=Kazuyasu kn-aut-name=藤井一恭 kn-aut-sei=藤井 kn-aut-mei=一恭 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END