Triggering CD101 molecule on human cutaneous dendritic cells inhibits T cell proliferation via IL-10 production

Since the CD101 molecule is expressed on a major subpopulation of HLA-DR+, CD1a(+), CD1c(+) cutaneous dendritic cells (DC), we studied the functional role of CD101 on cutaneous DC. Anti-CD101 monoclonal antibody (mAb) inhibit ed the proliferation of T cells induced by cutaneous DC. There was a synerg istic inhibition between anti-CD101 mAb and anti-CD86/ anti-CD80 mAb. Anti- CD101 mAb exerted its inhibitory effect when binding to the CD101 expressed on cutaneous DC. No positive role of CD101 putative ligand expressed by T cells in T cell proliferation was demonstrated, as T cells proliferated in response to soluble anti-CD3 mAb in the presence of CD86-transfected cells but not in the presence of CD101-transfected cells. Of major significance i s the fact that IL-10 was produced by cutaneous DC after CD101 triggering w ith anti-CD101 mAb, while IL-10 secretion was up-regulated in mixed cutaneo us DC-T cell cultures after CD101 triggering. Furthermore, IL-10-neutralizi ng mAb could reverse the inhibition induced by anti-CD101 mAb. Our results demonstrate that the CD101 triggering on cutaneous DC inhibits T cell proli feration via IL-10 production, suggesting an important regulatory role play ed by the CD101 molecule on DC during T cell activation.