AbstractThis study demonstrates that activation of human peripheral blood mononuclear cells (PBMC) by the T cell mitogens phytohemagglutinin (PHA) and concanavalin A (Con A) induces the expression of receptors for IgA without addition of IgA to the culture medium. Cells bearing receptors for IgA were determined by indirect immuno‐fluorescence using human secretory IgA and fluoresceinated goat anti‐human IgA or goat anti‐secretory component antibodies. Among freshly isolated PBMC, 4.7 ± 1.7% of T cells, 12.7 ± 12.5% of B cells and 14.4 ± 7.6% of monocytes were found to be IgA receptor positive. In unstimulated PBMC cultures the percentage of IgA receptor‐positive cells slightly increased at 48 h and was more elevated after 7 days. In Con A‐stimulated cultures 24.3 ± 18.5% of the cells expressed receptors for IgA after 48 h. Then, the number decreased and rose again thereafter. PHA stimulation induced an increase of smaller magnitude with similar kinetics. Induction of receptor for IgA on activated T cells was demonstrated by double‐labelling experiments showing more CD8+than CD4+cells with receptors for IgA among Con A‐activated PBMC. Furthermore, PHA or Con A stimulation of B cell‐depleted PBMC suspensions resulted in a marked increase of cells bearing receptors for IgA. Expression of these receptors was down‐regulated by recombinant interferon‐γ (250 units/ ml) and by prostaglandin PGE2(100 nM) both on unstimulated and mitogen‐activated PBMC. The receptor for IgA was distinct from the asialoglycoprotein receptor and did not cross‐react with the poly‐Ig receptor of epithelial cells. It was concluded that, in the absence of inducing exogenous IgA, T cell mitogens trigger the expression of receptors for IgA. Therefore, T cell activation is associated with the down‐regulation of receptors for IgM and the increased expression o
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