The effect of aging on IgD receptor expression by T cells and its functional implications

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Abstract
Summary: Exposure to oligomeric or aggregated (a), but not to mono‐merle (m), IgD causes a rapid (within 1 h) upregulation of IgD‐R expression on CD4+ T cells from young, but not from aged, mice and on both CD4+ and CD8+ T cells from all young and from =65% of aged humans. In normal young (but not in IgD−/‐) mice, this increase in IgD‐R expression is associated with a marked increase in primary and secondary antibody responses, transferable to both aged and young mice with T cells from aIgD pretreated donors. In both species, immunization causes a rise in the IgDR+ expression in vivo in the young. In mice, mIgD abolishes both the Induction of IgD‐R expression and augmentation of immune responses, suggesting that interaction between IgD‐R+ T and IgD+ B cells is needed. In aged humans, the ability of peripheral blood lymphocytes to exhibit IgD‐R expression in response to aIgD in vitro or to influenza vaccine in vivo is strongly correlated to the individual's ability to produce antibody. In T cells from aged mice, but not from aged IgD‐non‐responder humans, IgD‐R are able to come to the cell surface if an additional signal has been supplied, such as by (ionomycin/thapsigargin + aIgD). Agents which induce IgD‐R and augmentation of antibody production in aged and young mice include phosphatidylcholine and dehydroepiandrosterone sulfate. The immunoaugmenting effect of pretreatment with these agents appears Indeed due to IgD‐R+ T cells, because it is abolished by mIgD.