INTERLEUKIN-10, A NOVEL B-CELL STIMULATORY FACTOR - UNRESPONSIVENESS OF X-CHROMOSOME LINKED IMMUNODEFICIENCY-B CELLS

Highly purified, small dense splenic B cells from unstimulated mice showed increased expression of class II major histocompatibility complex (MHC) antigens and enhanced viability when cultured with affinity-purified recombinant interleukin 10 (HIA0), compared with B cells cultured in medium alone. These responses were blocked by a monoclonal antibody (mAb) specific for 11,10, but not by an isotype-matched control antibody. IL10 did not upregulate the expression of Fce receptors (CD23) or class I MHC antigens on small dense B cells or induce their replication as monitored by [3H]thymidine incorporation. While these B cell-stimulatory properties of IWO are also mediated by IL-4, the two cytokines appear to act independently in these assays ; anti- IL-10 antibodies blocked 1L-10 but not IL-4-mediated B cell viability enhancement, and vice versa. Similarly, since IL-4 upregulates CD23 on small dense B cells, the inability of IL-10 to do so argues against its acting via endogenously generated 114. Finally, IL-10 did not upregulate class II MHC antigens on B cells from X chromosome-linked immunodeficiency (XID) mice, while the same cells showed normal upregulation of class II antigens in response to 11.4. This report also extends our understanding of the relationship between IL-10 and the highly homologous Epstein-Barr virus (EBV)-encoded Barn HI fragment C rightward reading frame no. 1 (BCRFI) protein. It has previously been shown that BCRFIprotein exhibits the cytokine synthesis inhibitory activity of IL-10. This report indicates that BCRFI protein also enhances in vitroB cell viability, but does not upregulate class II MHC antigens on B cells. One explanation for these data is that IL-10 contains at least two functional epitopes, only one ofwhich has been conserved by EBV. © 1990, Rockefeller University Press., All rights reserved.