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Title: CXCR4 engagement promotes dendritic cell survival and maturation

Abstract

It has been reported that human monocyte derived-dendritic cells (DCs) express CXCR4, responsible for chemotaxis to CXCL12. However, it remains unknown whether CXCR4 is involved in other functions of DCs. Initially, we found that CXCR4 was expressed on bone marrow-derived DCs (BMDCs). The addition of specific CXCR4 antagonist, 4-F-Benzoyl-TN14003, to the culture of mouse BMDCs decreased their number, especially the mature subset of them. The similar effect was found on the number of Langerhans cells (LCs) but not keratinocytes among epidermal cell suspensions. Since LCs are incapable of proliferating in vitro, these results indicate that CXCR4 engagement is important for not only maturation but also survival of DCs. Consistently, the dinitrobenzene sulfonic acid-induced, antigen-specific in vitro proliferation of previously sensitized lymph node cells was enhanced by CXCL12, and suppressed by CXCR4 antagonist. These findings suggest that CXCL12-CXCR4 engagement enhances DC maturation and survival to initiate acquired immune response.

Authors:
 [1]; ;  [1];  [2];  [3];  [1]
  1. Department of Dermatology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555 (Japan)
  2. Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University, Chiyoda-ku, Tokyo 101-0062 (Japan)
  3. Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501 (Japan)
Publication Date:
OSTI Identifier:
21032915
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 361; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2007.07.128; PII: S0006-291X(07)01629-4; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANTIGENS; BONE MARROW; CELL PROLIFERATION; DENDRITES; IN VITRO; LYMPH NODES; MATURATION; MICE; MONOCYTES; SULFONIC ACIDS

Citation Formats

Kabashima, Kenji, Sugita, Kazunari, Shiraishi, Noriko, Tamamura, Hirokazu, Fujii, Nobutaka, and Tokura, Yoshiki. CXCR4 engagement promotes dendritic cell survival and maturation. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2007.07.128.
Kabashima, Kenji, Sugita, Kazunari, Shiraishi, Noriko, Tamamura, Hirokazu, Fujii, Nobutaka, & Tokura, Yoshiki. CXCR4 engagement promotes dendritic cell survival and maturation. United States. https://doi.org/10.1016/j.bbrc.2007.07.128
Kabashima, Kenji, Sugita, Kazunari, Shiraishi, Noriko, Tamamura, Hirokazu, Fujii, Nobutaka, and Tokura, Yoshiki. Fri . "CXCR4 engagement promotes dendritic cell survival and maturation". United States. https://doi.org/10.1016/j.bbrc.2007.07.128.
@article{osti_21032915,
title = {CXCR4 engagement promotes dendritic cell survival and maturation},
author = {Kabashima, Kenji and Sugita, Kazunari and Shiraishi, Noriko and Tamamura, Hirokazu and Fujii, Nobutaka and Tokura, Yoshiki},
abstractNote = {It has been reported that human monocyte derived-dendritic cells (DCs) express CXCR4, responsible for chemotaxis to CXCL12. However, it remains unknown whether CXCR4 is involved in other functions of DCs. Initially, we found that CXCR4 was expressed on bone marrow-derived DCs (BMDCs). The addition of specific CXCR4 antagonist, 4-F-Benzoyl-TN14003, to the culture of mouse BMDCs decreased their number, especially the mature subset of them. The similar effect was found on the number of Langerhans cells (LCs) but not keratinocytes among epidermal cell suspensions. Since LCs are incapable of proliferating in vitro, these results indicate that CXCR4 engagement is important for not only maturation but also survival of DCs. Consistently, the dinitrobenzene sulfonic acid-induced, antigen-specific in vitro proliferation of previously sensitized lymph node cells was enhanced by CXCL12, and suppressed by CXCR4 antagonist. These findings suggest that CXCL12-CXCR4 engagement enhances DC maturation and survival to initiate acquired immune response.},
doi = {10.1016/j.bbrc.2007.07.128},
url = {https://www.osti.gov/biblio/21032915}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 4,
volume = 361,
place = {United States},
year = {2007},
month = {10}
}