Aging is usually accompanied by diminished immune protection upon infection or vaccination. While aging results in well-characterized changes in the T-cell compartment of long-lived, outbred, and pathogen-exposed organisms, their relevance for primary antigen responses remain unclear. Therefore, it remains unclear whether and to what extent the loss of naïve T-cells, their partial replacement by oligoclonal memory populations, and the consequent constriction of T-cell receptor (TCR) repertoire, limit the antigen responses in aging primates.

Neonates are clearly more susceptible to severe disease following infection with a variety of pathogens than are adults. However, the causes for this are unclear and are often attributed to immunological immaturity. While several aspects of immunity differ between adults and neonates, the capacity of dendritic cells in neonates to process and present antigen to CD8+ T cells remains to be addressed. We used human CD8+ T cell clones to compare the ability of neonatal and adult monocyte-derived dendritic cells to present or process and present antigen using the MHC class I pathway. Specifically, we assessed the ability of dendritic cells to present antigenic peptide, present an HLA-E–restricted antigen, process and present an MHC class I-restricted antigen through the classical MHC class I pathway, and cross present cell-associated antigen via MHC class I. We found no defect in neonatal dendritic cells to perform any of these processing and presentation functions and conclude that the MHC class I antigen processing and presentation pathway is functional in neonatal dendritic cells and hence may not account for the diminished control of pathogens.