Accuri C6 Flow Cytometer System
Originally published online as doi:10.1189/jlb.0607357 on November 16, 2007

Published online before print November 16, 2007
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(Journal of Leukocyte Biology. 2008;83:439-446.)
© 2008 by Society for Leukocyte Biology

Dendritic cells at the interface of innate and acquired immunity: the role for epigenetic changes

Haitao Wen*, Matthew A. Schaller*, Yali Dou*,{dagger}, Cory M. Hogaboam* and Steven L. Kunkel*,1

* Departments of Pathology and
{dagger} Biological Chemistry, University of Michigan Medical School, Ann Arbor, Michigan, USA

1Correspondence: Department of Pathology, University of Michigan Medical School, 4071 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA. E-mail: slkunkel{at}umich.edu

ABSTRACT

Dendritic cells (DC) are known to be essential immune cells in innate immunity and in the initiation of adaptive immunity. The shaping of adaptive immunity by innate immunity is dependent on DC unique cellular functions and DC-derived effector molecules such as cytokines and chemokines. Thus, it is not surprising that numerous studies have identified alterations in DC number, function, and subset ratios in various diseases, such as infections, cancers, and autoimmune diseases. Recent evidence has also identified that immunosuppression occurring after severe systemic inflammation, such as found in sepsis, is a result of depletion in DC numbers and a later dysfunction in DC activity. This correlation suggests that the sustained DC dysfunction initiated by life-threatening inflammation may contribute to the subsequent immunoparalysis, potentially as a result of the long-term maintenance of an abnormal gene expression pattern. In this review, we summarized the present information regarding altered DC function after a severe, acute inflammatory response and propose a mechanism, whereby epigenetic changes can influence long-term gene expression patterns by DC, thus supporting an immunosuppression phenotype.

Key Words: sepsis • cytokine • Toll-like receptors • host defense • cell memory • long-term




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