SynCAM-dependent pathways may therefore represent novel points of therapeutic intervention after exposure to drugs of abuse. Neuropsychopharmacology (2013) 38, 628-638; doi:10.1038/npp.2012.226; published online 21 November 2012″
“A brief historical presentation of the hypothesis on receptor-receptor interactions as an important integrative BAY 73-4506 mw mechanism taking place at plasma membrane level is given. Some concepts derived from this integrative mechanism especially the possible assemblage of receptors in receptor mosaics (high-order
receptor oligomers) and their relevance for the molecular networks associated with the plasma membrane are discussed. In particular, the Rodbell’s disaggregation theory for G-proteins is revisited in the frame of receptor mosaic model.
The paper also presents some new indirect evidence on A2A boolean AND D2 receptor interactions obtained by means of Atomic Force Microscopy on immunogold preparations of A2A and D2 receptors in CHO cells. These findings support previous data obtained by means of computer-assisted confocal laser microscopy.
The allosteric control of G-protein coupled receptors is examined in the light of the new views on allosterism and recent
data on a homocysteine analogue capable of modulating D2 receptors are shown. Finally, the hypothesis is introduced on the existence of check-points learn more along the amino acid pathways connecting allosteric and orthosteric binding sites of a receptor and their potential importance for drug development. (C) 2009 Elsevier Ltd. All rights reserved.”
“T cell dysfunction in the presence of ongoing antigen exposure is a cardinal feature of chronic viral infections with persistent high viremia, including HIV-1. Although interleukin-10 (IL-10) has been implicated Prostatic acid phosphatase as an important mediator of this T cell dysfunction,
the regulation of IL-10 production in chronic HIV-1 infection remains poorly understood. We demonstrated that IL-10 is elevated in the plasma of individuals with chronic HIV-1 infection and that blockade of IL-10 signaling results in a restoration of HIV-1-specific CD4 T cell proliferation, gamma interferon (IFN-gamma) secretion, and, to a lesser extent, IL-2 production. Whereas IL-10 blockade leads to restoration of IFN-gamma secretion by HIV-1-specific CD4 T cells in all categories of subjects investigated, significant enhancement of IL-2 production and improved proliferation of CD4 T helper cells are restricted to viremic individuals. In peripheral blood mononuclear cells (PBMCs), this IL-10 is produced primarily by CD14(+) monocytes, but its production is tightly controlled by regulatory T cells (Tregs), which produce little IL-10 directly.