• Open Access

Nurine myeloid dendritic cell-dependent toll-like receptor immunity is preserved with aging


Daniel R. Goldstein, Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, 3 FMP, P.O. BOX 208017, New Haven, CT 06520-8018, USA. Tel.: 203 785 3271; fax: 203 785 7567; e-mail: daniel.goldstein@yale.edu


The immune response is the result of the interplay between innate and adaptive immunity, yet the impact of aging on this interaction is unclear. Addressing this fundamental question will be critical for the development of effective vaccines for the rapidly rising older subpopulation that manifests increased prevalence of malignancies and infections. Therefore, we undertook the current study to investigate whether aging impairs toll-like receptor (TLR) function in myeloid dendritic cells and whether this leads to reduced T-cell priming. Our results demonstrate that innate TLR immune priming function of myeloid bone marrow derived and splenic dendritic cells (DC) is preserved with aging using both allogeneic and infectious murine experimental systems. In contrast, aging impairs in vitro and in vivo intrinsic T-cell function. Therefore, our results demonstrate that myeloid DCs manifest preserved TLR-mediated immune responses with aging. However, aging critically impairs intrinsic adaptive T-cell function.