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,
,§
*
Laboratory of Oncology, G. Gaslini Institute, Genoa, Italy;
Wistar Institute of Anatomy and Biology, Philadelphia, PA 19104;
Division of Experimental Oncology, Istituto per lo Studio e la Cura dei tumori, Milan, Italy; and
§
Dynavax Technologies, Berkeley, CA 94705
IL-12 activates murine and human B cells, but little information is
available as to the expression and function of IL-12R on human B
lymphocytes. Here we show that the latter cells, freshly isolated from
human tonsils, expressed the transcripts of both ß1 and ß2 chains
of IL-12R and that ß2 chain mRNA was selectively increased (4- to
5-fold) by incubation with Staphylococcus aureus Cowan I
bacteria or IL-12. B cell stimulation with IL-12 induced de novo
expression of the transcripts of the two chains of IL-18R, i.e., IL-1
receptor-related protein and accessory protein-like. Functional studies
showed that both IL-12 and IL-18 signaled to B cells through the
NF-
B pathway. In the case of IL-12, no involvement of STAT
transcription factors, and in particular of STAT-4, was detected.
c-rel and p50 were identified as the members of NF-B
family involved in IL-12-mediated signal transduction to B cells. IL-12
and IL-18 synergized in the induction of IFN-
production by
tonsillar B cells, but not in the stimulation of B cell
differentiation, although either cytokine promoted IgM secretion in
culture supernatants. Finally, naive but not germinal center or memory,
tonsillar B cells were identified as the exclusive IL-12 targets in
terms of induction of NF-B activation and of IFN-
production.
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