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Kali
ski2,*
*
Department of Cell Biology and Histology and
Department of Dermatology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
IL-12 is a key inducer of Th1-associated inflammatory responses,
protective against intracellular infections and cancer, but also
involved in autoimmune tissue destruction. We report that human Th2
cells interacting with monocyte-derived dendritic cells (DC)
effectively induce bioactive IL-12p70 and revert to Th0/Th1 phenotype.
In contrast, the interaction with B cells preserves polarized Th2
phenotype. The induction of IL-12p70 in Th2 cell-DC cocultures is
prevented by IL-4-neutralizing mAb, indicating that IL-4 acts as a Th2
cell-specific cofactor of IL-12p70 induction. Like IFN-
, IL-4
strongly enhances the production of bioactive IL-12p70 heterodimer in
CD40 ligand-stimulated DC and macrophages and synergizes with IFN-
at low concentrations of both cytokines. However, in contrast to
IFN-, IL-4 inhibits the CD40 ligand-induced production of inactive
IL-12p40 and the production of either form of IL-12 induced by LPS,
which may explain the view of IL-4 as an IL-12 inhibitor. The presently
described ability of IL-4 to act as a cofactor of Th cell-mediated
IL-12p70 induction may allow Th2 cells to support cell-mediated
immunity in chronic inflammatory states, including cancer,
autoimmunity, and atopic dermatitis.
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