Innate immunity and aging

Abstract

Advanced age is associated with defects in all of the cells of the innate immune system, including numbers, function, and early stages of activation. This review, presents the current state of the field on the impact of age on the innate immune system. The analysis of the literature suggests that a dysfunctional innate immune system is a contributing factor to aberrant outcomes after injury or infection and to the development of many of the diseases observed in the elderly. Gaining an understanding of the nature of the defects in innate immune cells may allow the development of therapeutic strategies aimed to restore innate immune function in aged individuals.

Figure 1

Abbreviations: fMLP: N-formyl-methionyl-leucyl-phenylalanine; GM-CSF: granulocyte monocyte colony stimulating factor; TLR4: toll-like receptor 4; PMA: phorbol myristate acetate; ERK: extracellular signal regulated kinase; IP₃: inositol triphosphate; DAG: diacyl glycerol; cAMP: cyclic adenosine monophosphate; pTREM-1: triggering receptor expressed on myeloid cell-1.

Figure 2

Abbreviations: MHCII: major histocompatibility complex II; CD14: cluster of differentiation 14; TLR: toll-like receptor; COX-2: cyclooxygenase-2; STAT-1α: signal transducer and activator of transcription-1 alpha; MAPK: mitogen activated protein kinase; PKC: protein kinase C; NF-κB: nuclear factor-kappaB.