The analysis of 30 well characterized murine T lymphocyte populations using a cytofluorometric
IgA binding assay has identified many populations that are constitutive and/or inducible for
IgA receptor expression, and has identified two distinct mechanisms by which
IgA up-regulates the
IgA-binding properties of murine T cells. Studies with
lymphomas, hybridomas, Ag-specific clones and activated normal splenic T cells identified many examples of CD4 and CD8 lineage cells that constitutively expressed
IgA receptors. T cell populations that constitutively expressed
IgA receptors exhibited enhanced
IgA binding after incubation with oligomeric
IgA for 18 h. The
IgA-induced up-regulation of
IgA binding resulted from two distinct processes: 1) an increase in the number of surface membrane
IgA binding sites and 2) an increase in the avidity of
IgA binding without a change in the number of binding sites. The
IgA-induced avidity increase was reflected by a 5- to 10-fold decrease in the apparent Kd. Depending on the T cell population examined the enhanced binding of
IgA involved one or both of these mechanisms. T cell populations that did not constitutively express
IgA receptors failed to bind
IgA after prolonged incubation with oligomeric
IgA suggesting that if such cells can express
IgA receptors they require other signals to induce their expression. Consistent with this possibility is the finding that resting splenic T cells did not bind
IgA but their activation with Con A or mAb anti-T3 resulted in high level expression of
IgA receptors. These studies have identified multiple distinct mechanisms that alter the
IgA-binding properties of murine T cells and are discussed in terms of their possible physiologic significance.