Induction of latency-associated peptide (transforming growth factor-beta(1)) expression on CD4+T cells reduces Toll-like receptor 4 ligand-induced tumour necrosis factor-alpha production in a transforming growth factor-beta-dependent manner

CD4+ T cells expressing the latent form of transforming growth factor-beta [latency-associated peptide (LAP) (TGF-beta(1))] play an important role in the modulation of immune responses. Here, we identified a novel peptide ligand (GPC(81-95)) with an intrinsic ability to induce membrane-bound LAP (TGF-beta(1)) expression on a subpopulation of human CD4+ T cells (using flow cytometry; ranging from 0 center dot 8% to 2 center dot 6%) and stimulate peripheral blood mononuclear cells to release LAP (TGF-beta(1)) (using ELISPOT assay; ranging from 0 center dot 03% to 0 center dot 16%). In spite of this low percentage of responding cells, GPC(81-95) significantly reduced Toll-like receptor 4 ligand-induced tumour necrosis factor-alpha production in a TGF-beta(1)- and CD4+ T-cell-dependent manner. The results demonstrate that GPC(81-95) is a useful tool to study the functional properties of a subpopulation of LAP (TGF-beta(1))+ CD4+ T cells and suggest a pathway that can be exploited to suppress inflammatory response.