26 research outputs found

    THE CONCISE GUIDE TO PHARMACOLOGY 2021/22: G protein-coupled receptors.

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    The Concise Guide to PHARMACOLOGY 2021/22 is the fifth in this series of biennial publications. The Concise Guide provides concise overviews, mostly in tabular format, of the key properties of nearly 1900 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties. Although the Concise Guide constitutes over 500 pages, the material presented is substantially reduced compared to information and links presented on the website. It provides a permanent, citable, point-in-time record that will survive database updates. The full contents of this section can be found at http://onlinelibrary.wiley.com/doi/bph.15538. G protein-coupled receptors are one of the six major pharmacological targets into which the Guide is divided, with the others being: ion channels, nuclear hormone receptors, catalytic receptors, enzymes and transporters. These are presented with nomenclature guidance and summary information on the best available pharmacological tools, alongside key references and suggestions for further reading. The landscape format of the Concise Guide is designed to facilitate comparison of related targets from material contemporary to mid-2021, and supersedes data presented in the 2019/20, 2017/18, 2015/16 and 2013/14 Concise Guides and previous Guides to Receptors and Channels. It is produced in close conjunction with the Nomenclature and Standards Committee of the International Union of Basic and Clinical Pharmacology (NC-IUPHAR), therefore, providing official IUPHAR classification and nomenclature for human drug targets, where appropriate

    Requirement for hla-dr + accessory cells in natural killing of cytomegalovirus-infected fibroblasts

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    NK cells mediate spontaneous killing of tumor-derived cells, virus-infected cells, and certain normal cells (1, 2). This type of cytotoxicity does not require presensitization of the donor. For example, PBMC of individuals who are seronegative or seropositive for a given virus are equally able to lyse targets infected with that virus (3). Production of IFN by lymphocytes exposed to virusinfected target cells and subsequent stimulation of NK cells by IFN was originally proposed as the mechanism by which NK cells preferentially lyse virus-infected cells compared with uninfected ones (4). A primary role for IFN was challenged, however, by several authors who described a lack of correlation between magnitude of lysis and amounts of IFN detected in supernatant fluids (5, 6), an almost normal capacity of effector cells from patients with reduced ability to produce IFN to lyse virus-infected target cells (7), and the inability of anti-IFN antibodies when present during the NK assay to prevent lysis of virus-infected cells (5, 6). The cells responsible for NK activity against normal and tumor-derived target cell lines were identified as a leukocyte subset, distinct from B and T cells and from myelomonocytic cells (2). This subset expresses the low-affinity Fc receptor (FcR) 1 for aggregated IgG (CD16 antigen), recognized by a series of mAbs (8). NK cells responsible for lysis of virus-infected target cells have not been fully identified. Fitzgerald et al. (9) reported that the NK cells able to lyse HSVinfected targets differed from those that lysed K562 cells, as treatment of PBMC with an mAb to HLA-DR plus C reduced their ability to kill HSV-infected fibroblasts, but not K562 cells. These authors concluded that these NK cell subsets could be distinguished on the basis of surface expression of HLA-DR antigen. However, few if any resting NK (CD16+) cells in healthy donors are HLA-DR + (10, 1 1), raising the possibility that in the experiments of Fitzgerald et a]. (9), a HLA-DR +, non-NK cell population was depleted
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