Virulence is a rare outcome of infection, occurring in fewer than 1 in 10 infections. Not all strains of the parasite are equally virulent, and understanding the mechanisms and causes of virulence is an important goal of Entamoeba
research. The sequencing of the genome of E. histolytica and the related avirulent species Entamoeba dispar has allowed selleck chemicals llc whole-genome-scale analyses of genetic divergence and differential gene expression to be undertaken. These studies have helped elucidate mechanisms of virulence and identified genes differentially expressed in virulent and avirulent parasites. Here, we review the current status of the E. histolytica and E. dispar genomes and the findings of a number of genome-scale studies comparing parasites of different virulence. “
“CD4+ T cells expressing the latent form of transforming growth factor-β [latency-associated peptide (LAP) (TGF-β1)] play an important role in the modulation of immune responses. Here, we identified a novel peptide ligand (GPC81–95) with an intrinsic ability to induce membrane-bound LAP (TGF-β1) expression on a subpopulation of human CD4+ T cells (using flow cytometry; ranging from 0·8% to 2·6%) and stimulate peripheral blood mononuclear cells to release LAP (TGF-β1) (using ELISPOT assay; ranging from 0·03%
to 0·16%). In spite of this low percentage of responding cells, GPC81–95 significantly reduced Toll-like receptor 4 ligand-induced tumour necrosis factor-α
production in a TGF-β1- and CD4+ T-cell-dependent CP-690550 molecular weight manner. The results demonstrate that GPC81–95 is a useful tool to study the functional properties of a subpopulation of LAP (TGF-β1)+ CD4+ T cells and suggest a pathway that can be exploited to suppress inflammatory response. Transforming growth factor-β1 (TGF-β1) is involved in the regulation of numerous cellular functions and is produced by most cell types in a latent form. The latent form of TGF-β1 [LAP (TGF-β1)] is comprised of latency-associated peptide (LAP) non-covalently bound to mature TGF-β1. It is known that many immune cells can produce LAP (TGF-β1) or can express this molecule on their cell surface1,2 and that LAP (TGF-β1)-expressing CD4+ T cells play an important role in modulation of immune responses.3–5 It has been shown that oral or nasal administration of anti-CD3 4-Aminobutyrate aminotransferase antibodies induces LAP (TGF-β1)+ CD4+ T cells and suppresses autoimmune disease in animal models in a TGF-β1-dependent manner,3,6 but there is little information on other LAP (TGF-β1)-inducing ligands or the mechanism involved in the induction of this regulatory molecule on CD4+ T cells. Tumour necrosis factor-α (TNF-α) is a pro-inflammatory cytokine that is produced mainly by monocytes and macrophages after stimulation with endotoxin.7 It has many immunostimulatory functions and plays a crucial role in inflammation and immunity.