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7. Murine [corrected] myeloid dendritic cell-dependent toll-like receptor immunity is preserved with aging.

Author

Tesar BM, Walker WE, Unternaehrer J, Joshi NS, Chandele A, Haynes L, Kaech S, and Goldstein DR

Subjects
Adaptation, Physiological immunology, Animals, Antigen Presentation immunology, Immune System physiopathology, Immunity, Innate immunology, Lymphocytic Choriomeningitis immunology, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Myeloid Cells cytology, Myeloid Cells immunology, Spleen cytology, Spleen immunology, Aging immunology, Dendritic Cells immunology, Immune System immunology, Immunity, Cellular immunology, T-Lymphocytes immunology, Toll-Like Receptors immunology
Abstract

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.

Published
2006
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