Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0408257 on February 19, 2009

Published online before print February 19, 2009
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(Journal of Leukocyte Biology. 2009;85:862-870.)
© 2009 Society for Leukocyte Biology

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*,1

* 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

1 Correspondence: Department of Surgery (Immunology), Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA. E-mail: jlederer{at}rics.bwh.harvard.edu

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. We also 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