Tissue-resident DCs continually survey and sample their local environment for invading microbes, whose recognition triggers DC maturation and their migration to secondary lymphoid organs. Both human and murine-based studies have demonstrated a significant impairment in DC migration with age [76, 81]. The age- associated aberration in the in vivo migration of murine DCs has been attributed to an altered microenvironment as well as impaired signalling from surface expressed chemokine receptors [81, 82].
Increasing experimental evidence suggests that the stimulatory capacity of mDCs wanes with age. Compared to those isolated from young controls, aged mDCs are less effective at inducing T cell proliferation [78,81,83], IFN-y secretion [83, 84] and T cell cytotoxicity [81, 84], defects that would be expected to lead to a diminished T cell-mediated immune response. However, with several studies reporting that antigen presentation and expression of the co-stimulatory molecules CD80/86 are comparable between DCs following stimulation, it cannot be ruled out that the weakened T cell response of aged individuals may be the result of consequence of intrinsic T cell defects rather than impaired DC function .
Whether ageing is associated with alterations in pro-inflammatory cytokine production by mDCs is an area of controversy, with studies reporting increased , decreased [75,86] or comparable  generation of TNF-a, IL-6 and IL-12 by aged mDCs in response to TLR stimulation when compared to that secreted by young mDCs. Studies that have reported a decline in cytokine production have attributed it to an age-related reduction in TLR expression , impaired intracellular signalling  and an age-associated increase in basal cytokine levels .