Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Munster, D. J.
Right arrow Articles by Hart, D. J. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Munster, D. J.
Right arrow Articles by Hart, D. J. N.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 16, No. 1, pp. 33-42, January 2004
© 2004 Japanese Society for Immunology

Human T lymphoblasts and activated dendritic cells in the allogeneic mixed leukocyte reaction are susceptible to NK cell-mediated anti-CD83-dependent cytotoxicity

David J. Munster1, Kelli P. A. MacDonald1,2, Masato Kato1 and Derek J. N. Hart1

1 Dendritic Cell Laboratory, Mater Medical Research Institute, Brisbane, Queensland 4101, Australia 2 Present address: Immunoregulation Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Royal Brisbane Hospital, Queensland 4029, Australia

Correspondence to: D. N. J. Hart; E-mail: dhart{at}mmri.mater.org.au
Transmitting editor: D. Tarlinton

CD83 is a marker of dendritic cell (DC) differentiation/activation and its expression in the mouse thymus contributes to CD4+ T lymphocyte development. Its extrathymic role remains unclear despite the functional effects observed with CD83 fusion proteins or CD83 antibody and recent reports of potential ligands. We investigated the previously observed and presumed functional blockade of the allogeneic mixed leukocyte reaction (MLR) with rabbit polyclonal anti-CD83 (RA83). RA83 inhibition of T lymphocyte proliferation stimulated with allogeneic immature monocyte-derived DC (iMoDC) was confirmed. However, we found it was due to antibody-dependent cellular cytotoxicity (ADCC) mediated by NK cells in the responder T cell preparation. The likely targets of the ADCC were MoDC that had up-regulated CD83 during the MLR. Using a 51Cr-release assay, we confirmed that CD83+ MoDC, but not CD83 MoDC, are lysed by NK cells in the presence of RA83. However, prior fixation of the stimulator MoDC in the allogeneic MLR did not abrogate RA83 inhibition, indicating that cells from the responder T lymphocyte preparation, involved in the MLR proliferative response, also expressed CD83. We found, after 3–4 days of culture with allogeneic MoDC, a subset of CD3+ cells had up-regulated CD83 and CD25. These were blasting T cells and, when isolated from the MLR, were found to be lysed by autologous NK cells in the presence of RA83. Thus, CD83 is expressed by responding T cells as well as by stimulating cells in the MLR and both are susceptible to anti-CD83-mediated ADCC.

Keywords: cellular activation, immunosuppression, mixed leukocyte reaction, T lymphocyte


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Immunol.Home page
C. M. Prazma, N. Yazawa, Y. Fujimoto, M. Fujimoto, and T. F. Tedder
CD83 Expression Is a Sensitive Marker of Activation Required for B Cell and CD4+ T Cell Longevity In Vivo
J. Immunol., October 1, 2007; 179(7): 4550 - 4562.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
E. Klein, S. Koch, B. Borm, J. Neumann, V. Herzog, N. Koch, and T. Bieber
CD83 localization in a recycling compartment of immature human monocyte-derived dendritic cells
Int. Immunol., April 1, 2005; 17(4): 477 - 487.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.