  Cells of the immune system are confronted with opposing pro- and
anti-inflammatory signals. Dendritic cells (DC) integrate these cues to make
informed decisions whether to initiate an immune response. Confronted with
exogenous microbial stimuli, DC endogenously produce both anti- (IL-10) and
pro-inflammatory (TNF$\alpha$) cues whose joint integration controls the cell's
final decision. We combine experimental measurements with theoretical modeling
to quantitatively describe the integration mode of these opposing signals. We
propose a two step integration model that modulates the effect of the two types
of signals: an initial bottleneck integrates both signals (IL-10 and
TNF$\alpha$), the output of which is later modulated by the anti-inflammatory
signal. We show that the anti-inflammatory IL-10 signaling is long ranged, as
opposed to the short-ranged pro-inflammatory TNF$\alpha$ signaling. The model
suggests that the population averaging and modulation of the pro-inflammatory
response by the anti-inflammatory signal is a safety guard against excessive
immune responses.
