Blackwell Publishing Journal Backfiles 1879-2005
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.
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