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Article
The B subunit of Escherichia coli heat-labile toxin alters the development and antigen-presenting capacity of dendritic cells
Journal of Cellular and Molecular Medicine
  • Jing Ji, Australian National University
  • Kristin Grifftiths, Australian National University
  • Peter Milburn, Australian National University
  • Timothy Hirst, Australian National University
  • Helen O'Neill, Bond University
Date of this Version
1-1-2015
Document Type
Journal Article
Grant Number
NHMRC project grant # 585443
Publication Details

Published Version

Ji, J., Griffiths, K. L., Milburn, P. J., Hirst, T. R., & O'Neill, H. C. (2015). The B subunit of escherichia coli heat-labile toxin alters the development and antigen-presenting capacity of dendritic cells. Journal of Cellular and Molecular Medicine, 19(8), 2019-2031.

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© Copyright, The Authors, 2015

2015 HERDC Submission

Abstract
Escherichia coli's heat-labile enterotoxin (Etx) and its non-toxic B subunit (EtxB) have been characterized as adjuvants capable of enhancing T cell responses to co-administered antigen. Here, we investigate the direct effect of intravenously administered EtxB on the size of the dendritic and myeloid cell populations in spleen. EtxB treatment appears to enhance the development and turnover of dendritic and myeloid cells from precursors within the spleen. EtxB treatment also gives a dendritic cell (DC) population with higher viability and lower activation status based on the reduced expression of MHC-II, CD80 and CD86. In this respect, the in vivo effect of EtxB differs from that of the highly inflammatory mediator lipopolysaccharide. In in vitro bone marrow cultures, EtxB treatment was also found to enhance the development of DC from precursors dependent on Flt3L. In terms of the in vivo effect of EtxB on CD4 and CD8 T cell responses in mice, the interaction of EtxB directly with DC was demonstrated following conditional depletion of CD11c+ DC. In summary, all results are consistent with EtxB displaying adjuvant ability by enhancing the turnover of DC in spleen, leading to newly mature myeloid and DC in spleen, thereby increasing DC capacity to perform as antigen-presenting cells on encounter with T cells.
Citation Information
Jing Ji, Kristin Grifftiths, Peter Milburn, Timothy Hirst, et al.. "The B subunit of Escherichia coli heat-labile toxin alters the development and antigen-presenting capacity of dendritic cells" Journal of Cellular and Molecular Medicine Vol. 19 Iss. 8 (2015) p. 2019 - 2031 ISSN: 1582-4934
Available at: http://works.bepress.com/helen_oneill/24/