IFN-alpha-mediated suppression of low-affinity FC(epsilon) receptors on Peyer's patch lymphocytes and augmentation of soluble CD23: implications for IgE responses

The ability of interleukin (IL)‐6 or interferon‐α (IFN‐α) to regulate expression of low‐affinity Fc receptor (CD23) and serum levels of CD23 was studied in benzylpenicilloyl‐keyhole limpet hemocyanin‐sensitized BALB/c mice at the peak of a haptenspecific immunoglobulin E (IgE) antibody‐forming cell (AFC) response. These responses are analogous to those observed in human atopic disease. To induce peak IgE responses, mice were injected intraperitoneally with BPO‐KLH (10 μg) in aluminum hydroxide gel (alum) on days 0, 21, and 42. On day 44, mice were injected subcutaneously with IL‐6 (100‐1000 U) or IFN‐α (1000‐10,000 U). On day 46, numbers of CD23+ lymphocytes in Peyer's patches (PP), mesenteric lymph nodes (MLN), and spleen and levels of soluble CD23 in serum were determined (flow microfluorimetry and enzyme‐linked immunosorbent assay, confirmed by competition assay). Data are expressed as percent total cells or as optical density at 490 nm. IFN‐α treatment strongly suppressed (up to 100%) numbers of CD23+ cells exclusively in PP (i.e., numbers of CD23+ cells in MLN and spleen were unchanged) whereas serum levels of soluble CD23 were dramatically increased (60%). IL‐6 treatment had no effect on either numbers of CD23+ lymphocytes or on serum levels of soluble CD23. The data suggest that the mechanism(s) by which IFN‐α, but not IL‐6, regulates IgE responses involves suppression of CD23 expression on lymphocytes in PPs and supports a central role for these organs in regulation of IgE responses in vivo.