Fig. 1.

(A) Chemical structures of d-glucosamine and melibiosamine. (B) Hypothetical scheme for the signaling cascades leading to the expression of interleukin (IL)-2 mRNA in Jurkat cells and the actions of GlcNH₂ and MelNH₂. The mitogen concanavalin A (ConA) stimulates IL-2 production via T-cell receptor (TCR) and subsequent activation of the calcineurin/nuclear factor of activated T-cells (CN/NFAT), IκB kinase/nuclear factor kappa-light-chain-enhancer of activated B cells (IKK/NFκB), and mitogen-activated protein kinase/activator protein 1 (MAPK/AP-1) pathways. The immunosuppressive drugs cyclosporine A (CsA) and tacrolimus (FK506) inhibit CN via immunophilins. It was assumed that phorbol 12-myristate 13-acetate (PMA) and ionomycin (IM) together mimic the actions of ConA with regard to the induction of IL-2 expression in vitro. MelNH₂ and GlcNH₂ suppress the activation of NFATc1 and NFκB by ConA, whereas MelNH₂, but not GlcNH₂, promotes the activation of AP-1. PM, plasma membrane; PLC, phospholipase C; IP₃, inositol 1,4,5-trisphosphate; DAG, diacylglycerol; PKC, protein kinase C. ‘P-’ indicates phosphate group, and the gray arrow inside the nucleus indicates IL-2 transcription.