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タイトル: | Neonatal Fc receptor induces intravenous immunoglobulin growth suppression in Langerhans cell histiocytosis |
著者: | Nabeshima, Yuka Kataoka, Tatsuki R. Ueshima, Chiyuki Saito, Narumi Hirata, Masahiro Takeuchi, Yasuhide Takei, Yusuke Moriyoshi, Koki Ono, Kazuo Haga, Hironori |
著者名の別形: | 鍋島, 優香 片岡, 竜貴 上島, 千幸 平田, 勝啓 竹内, 康英 竹井, 雄介 森吉, 弘毅 羽賀, 博典 |
キーワード: | albumin cell growth intravenous immunoglobulin Langerhans cell histiocytosis neonatal Fc receptor |
発行日: | Mar-2021 |
出版者: | Wiley |
誌名: | Pathology International |
巻: | 71 |
号: | 3 |
開始ページ: | 191 |
終了ページ: | 198 |
抄録: | The neonatal Fc receptor (FcRn) plays a role in trafficking IgG and albumin and is thought to mediate intravenous immunoglobulin (IVIG) therapy for certain diseases. IVIG can be used for the treatment of human Langerhans cell histiocytosis (LCH); however, the mechanism remains unclear. The expression and function of FcRn protein have not been studied in LCH, though the expression of FcRn messenger RNA (mRNA) have been reported. In this report, we confirmed the expression of FcRn in 26 of 30 pathological cases (86.7%) diagnosed immunohistochemically as LCH. The expression was independent of age, gender, location, multi- or single-system, and the status of BRAFV600E immunostaining. We also confirmed the expression of FcRn mRNA and protein in the human LCH-like cell line, ELD-1. FcRn suppressed albumin consumption and growth of IVIG preparation-treated ELD-1 cells, but not of IVIG preparation-untreated or FcRn-knockdown ELD-1 cells. In addition, FITC-conjugated albumin was taken into Rab11-positive recycle vesicles in mock ELD-1 cells but not in FcRn-knockdown ELD-1 cells. IVIG preparation prolonged this status in mock ELD-1 cells. Therefore, ELD-1 recycled albumin via FcRn and albumin was not used for metabolism. Our results increase our understanding of the molecular mechanism of IVIG treatment of LCH. |
著作権等: | © 2021 The Authors. Pathology International published by Japanese Society of Pathology and John Wiley & Sons Australia, Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
URI: | http://hdl.handle.net/2433/276572 |
DOI(出版社版): | 10.1111/pin.13068 |
PubMed ID: | 33497038 |
出現コレクション: | 学術雑誌掲載論文等 |
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