Ribotoxic stress activates p38 and JNK kinases and modulates the antigen-presenting activity of dendritic cells.

Initiation of adaptive immunity requires activation of dendritic cells (DC) by "danger" signals. This study examines the functional consequences of activating a cellular stress response in human DC. Anisomycin, a potent inducer of this "stress" response, selectively activates p38 kinase in DC at low concentrations, and both p38 kinases and JNKs at higher concentrations.

Effects of oxidised low density lipoprotein on dendritic cells: a possible immunoregulatory component of the atherogenic micro-environment?

Objective: The objective of this study was to explore the relationship between low density lipoprotein (LDL) and dendritic cell (DC) activation, based upon the hypothesis that reactive oxygen species (ROS)-mediated modification of proteins that may be present in local DC microenvironments could be important as mediators of this activation. Although LDL are known to be oxidised in vivo, and taken up by macrophages during atherogenesis; their effect on DC has not been explored previously.

Methods: Human DCs were prepared from peripheral blood monocytes using GM-CSF and IL-4.

The role of advanced oxidation protein products in regulation of dendritic cell function.

The basis for this study was the "injury hypothesis," which holds that release of micro-environmental constituents, such as reactive oxygen species and oxidants, acts as a signal, and potential activator, of dendritic cell (DC)-mediated antigen presentation. Following this oxidative stress, dityrosine containing cross-linked proteins, advanced oxidation protein products (AOPP), are known to be generated, and we proposed that they may serve as moieties that mediate such signals. Therefore, the effect of AOPP on DCs has been examined in vitro.