Pepro Tech
A more recent version of this article appeared on May 1, 2009

Published online before print February 19, 2009
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0408257v1
85/5/862    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fujimi, S.
Right arrow Articles by Lederer, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fujimi, S.
Right arrow Articles by Lederer, J. A.
© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0408257

Received for publication April 23, 2008.
Revised December 2, 2008.
Accepted for publication December 22, 2008.

Article

Murine dendritic cell antigen-presenting cell function is not altered by burn injury

Satoshi Fujimi *, Peter H. Lapchak {dagger}, Yan Zang *, Malcolm P. MacConmara *, Adrian A. Maung *{ddagger}, Adam J. Delisle *, John A. Mannick *, and James A. Lederer *@

*Department of Surgery (Immunology), Brigham and Women’s Hospital, and {dagger}Department of Medicine/Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA; and {ddagger}Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts, USA

@ To whom correspondence should be addressed. E-mail: jlederer{at}rics.bwh.harvard.edu.


arrow
Abstract

Severe injury disrupts normal immune regulation causing a transient hyperinflammatory reaction and suppressed adaptive immune function. This report addresses the potential contribution of dendritic cells (DC) to changes in adaptive immune function after injury by specifically measuring injury-induced changes in splenic DC numbers and subsets, cell-surface markers, TLR responses, and APC function. Using a mouse burn injury model, we found that injury did not markedly alter the relative percentage of lymphoid, myeloid, or plasmacytoid DC in the spleens of burn-injured mice. Moreover, we did not observe a significant reduction in cell-surface expression of several major costimulatory molecules, CD40, CD80, CD86, programmed death 1 ligand, ICOS ligand, and B7-H3, on DC. Instead, we observed increased cell-surface expression of CD86 at 1 day after injury with no significant changes in costimulatory molecule expression at 7 days after injury, suggesting that burn injury causes an early activation of DC. In addition, injury did not suppress DC reactivity to TLR2, TLR4, or TLR9 agonists. Most important, DC prepared from injured mice were able to present peptide antigen to naïve OTII TCR transgenic CD4+ T cells as efficiently and effectively as DC from sham-injured mice. In addition, we found that CD4 T cells stimulated with antigen presented by DC from sham or burn mice showed similar levels of IL-2, IFN-{gamma}, IL-10, and IL-13 production. Taken together, these findings support the conclusion that DC do not acquire a suppressive phenotype following severe injury in mice.

Key Words: Toll-like receptors • costimulatory molecules • Th1 • Th2 • CD4 T cells