Reveromycin A Inhibits Antigen Receptor-mediated Antigen Presentation by B Lymphoma Cells via Its Effect on Intracellular Trafficking of the Antigen.
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- TANAKA YURIKO
- Department of Immunology, Toho University School of Medicine
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- ISHIKAWA FUMIO
- Department of Immunology, Toho University School of Medicine
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- OSADA HIROYUKI
- Antibiotic Laboratory, The Institute of Physical and Chemical Research (RIKEN)
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- IMAJOH-OHMI SHINOBU
- Department of Basic Medical Science, The Institute of Medical Science, The University of Tokyo
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- UCHIDA TETSUYA
- Department of Safety Research on Biologics, National Institute of Infectious Disease
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- KAKIUCHI TERUTAKA
- Department of Immunology, Toho University School of Medicine
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Reveromycin A (Rev.A) is an inhibitor of epidermal growth factor-dependent cell growth that is produced from the culture broth of an actinomycete strain. Rev.A was assessed for its ability to regulate antigen (Ag) presentation by A20-HL B lymphoma cells bearing trinitrophenyl (TNP)-specific surface IgM (sIgM) to cloned T cells specific for OVA323-339/I-Ad. Rev.A-treatment inhibited the presentation of Ag internalized via sIgM, but not of Ag via fluid-phase pinocytosis. Rev.A-treatment decreased protein synthesis, but a similar decrease in protein synthesis by cycloheximide induced much less inhibition of sIgM-mediated Ag presentation. Rev.A-treatment decreased the rate of re-expression of sIgM in A20-HL cells, the amount of Ag internalized via sIgM during 3 hours of incubation, and the generation of antigenic peptides from TNP-OVA internalized via sIgM. Rev.A-treatment was suggested to affect intracellular trafficking from early endosomes into late endocytic compartments of Ag internalized via sIgM. Rev.A might provide a useful tool for studying intracellular transport of Ag, especially Ag internalized via sIgM.
収録刊行物
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- The Journal of Antibiotics
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The Journal of Antibiotics 55 (10), 904-913, 2002
公益財団法人 日本感染症医薬品協会
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詳細情報 詳細情報について
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- CRID
- 1390282679127143680
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- NII論文ID
- 130003503929
- 50000674021
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- NII書誌ID
- AA0069330X
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- COI
- 1:CAS:528:DC%2BD38XotlChs70%3D
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- ISSN
- 18811469
- 00218820
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- PubMed
- 12523824
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 使用不可