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   <subfield code="a">10.1007/s00535-011-0460-4</subfield>
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   <subfield code="a">Amelioration of 2,4,6-trinitrobenzene sulfonic acid-induced colitis in mice by immunoregulatory dendritic cells</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Shoichi Hoshino, Akiko Kurishima, Muneo Inaba, Yugo Ando, Toshiro Fukui, Kazushige Uchida, Akiyoshi Nishio, Hiroshi Iwai, Takashi Yokoi, Tomoki Ito, Sanae Hasegawa-Ishii, Atsuyoshi Shimada, Ming Li, Kazuichi Okazaki, Susumu Ikehara]</subfield>
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   <subfield code="a">Background: Dendritic cells (DCs) are widely distributed throughout the lymphoid and nonlymphoid tissues, and are important initiators of acquired immunity. They also serve as regulators by inducing self-tolerance. However, it has not been thoroughly clarified whether DCs are somehow involved in the regulation or treatment of inflammatory bowel diseases. Methods: We established an ileitis model by transmurally injecting 2,4,6-trinitrobenzene sulfonic acid (TNBS) into the lumen of the ileocolonic junction. The kinetic movement of DCs at the inflammatory sites was analyzed histologically and by flow cytometry, and DCs obtained from the small intestine were analyzed in order to determine the expression of paired immunoglobulin-like receptor-A/B (PIR-A/B) by flow cytometry and quantitative RT-PCR. Furthermore, the regulatory role of DCs was directly determined by a transfer experiment using TNBS-induced colitis model mice. Results: We observed three DC subsets (PIR-A/Bhigh, PIR-A/Bmed, and PIR-A/B− DCs) in the conventional DCs (cDCs) from day 3, and the number of PIR-A/Bmed cDCs increased from the time the inflammatory responses ceased (day 7). PIR-A/Bmed cDCs actually migrated to the inflamed colon, and ameliorated the colitis induced by TNBS when transferred to colitis-induced recipients. The colitis was greatly exacerbated when mice had been treated with the indoleamine-pyrrole 2,3-dioxygenase (IDO) inhibitor 1-methyltryptophan (1-mT) at the time PIR-A/Bmed cDCs were transferred, indicating that the therapeutic ability of PIR-A/Bmed cDCs is partially dependent on IDO. Conclusion: The PIR-A/Bmed cDCs, which increase in number during the final stages of inflammation, can be used to treat colitis via an IDO-dependent mechanism.</subfield>
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   <subfield code="a">Springer, 2011</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Dendritic cells</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Paired immunoglobulin-like receptors</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">TNBS</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Inflammatory bowel disease</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hoshino</subfield>
   <subfield code="D">Shoichi</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Kurishima</subfield>
   <subfield code="D">Akiko</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Inaba</subfield>
   <subfield code="D">Muneo</subfield>
   <subfield code="u">First Department of Pathology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Ando</subfield>
   <subfield code="D">Yugo</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Fukui</subfield>
   <subfield code="D">Toshiro</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Uchida</subfield>
   <subfield code="D">Kazushige</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Nishio</subfield>
   <subfield code="D">Akiyoshi</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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   <subfield code="a">Iwai</subfield>
   <subfield code="D">Hiroshi</subfield>
   <subfield code="u">Department of Otolaryngology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Yokoi</subfield>
   <subfield code="D">Takashi</subfield>
   <subfield code="u">First Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Ito</subfield>
   <subfield code="D">Tomoki</subfield>
   <subfield code="u">First Department of Internal Medicine, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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   <subfield code="a">Hasegawa-Ishii</subfield>
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   <subfield code="u">Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, Kasugai, Aichi, Japan</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Shimada</subfield>
   <subfield code="D">Atsuyoshi</subfield>
   <subfield code="u">Department of Pathology, Institute for Developmental Research, Aichi Human Service Center, Kasugai, Aichi, Japan</subfield>
   <subfield code="4">aut</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Li</subfield>
   <subfield code="D">Ming</subfield>
   <subfield code="u">Department of Stem Cell Disorders, Kansai Medical University, 10-15 Fumizono-cho, 570-8506, Moriguchi, Osaka, Japan</subfield>
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  <datafield tag="700" ind1="1" ind2=" ">
   <subfield code="a">Okazaki</subfield>
   <subfield code="D">Kazuichi</subfield>
   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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   <subfield code="a">Ikehara</subfield>
   <subfield code="D">Susumu</subfield>
   <subfield code="u">Department of Stem Cell Disorders, Kansai Medical University, 10-15 Fumizono-cho, 570-8506, Moriguchi, Osaka, Japan</subfield>
   <subfield code="4">aut</subfield>
  </datafield>
  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Journal of Gastroenterology</subfield>
   <subfield code="d">Springer Japan</subfield>
   <subfield code="g">46/12(2011-12-01), 1368-1381</subfield>
   <subfield code="x">0944-1174</subfield>
   <subfield code="q">46:12&lt;1368</subfield>
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   <subfield code="2">46</subfield>
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   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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   <subfield code="u">The Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Moriguchi, Osaka, Japan</subfield>
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