Like children alive when their parents have not been born, there is a population of natural killer (NK) cells which appear to be self-renewing, according to 2 articles in this issue of . Corat et al and Schlums et al take us closer to this mystery by answering the question: is ongoing production from hematopoietic stem and progenitor cells (HSPCs) required to maintain NK-cell homeostasis in humans?
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| http://dx.doi.org/10.1182/blood-2016-12-755546 | DOI Listing |
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Like children alive when their parents have not been born, there is a population of natural killer (NK) cells which appear to be self-renewing, according to 2 articles in this issue of . Corat et al and Schlums et al take us closer to this mystery by answering the question: is ongoing production from hematopoietic stem and progenitor cells (HSPCs) required to maintain NK-cell homeostasis in humans?
View Article and Find Full Text PDFThe Orphan Receptor GPR17 Is Unresponsive to Uracil Nucleotides and Cysteinyl Leukotrienes.
Mol Pharmacol
May 2017
Molecular, Cellular and Pharmacobiology Section, Institute of Pharmaceutical Biology (K.S., N.M., Ral.S., S.H., P.P., N.-K.S, L.P., J.G., E.K.), Research Training Group 1873 (K.S., E.K.), Pharmacology and Toxicology Section, Institute of Pharmacy (Ram.S., K.M.), University of Bonn, Bonn, Germany; UCB Pharma, CNS Research, Braine l'Alleud, Belgium (C.V., M.G.).
Pairing orphan G protein–coupled receptors (GPCRs) with their cognate endogenous ligands is expected to have a major impact on our understanding of GPCR biology. It follows that the reproducibility of orphan receptor ligand pairs should be of fundamental importance to guide meaningful investigations into the pharmacology and function of individual receptors. GPR17 is an orphan receptor characterized by some as a dualistic uracil nucleotide/cysteinyl leukotriene receptor and by others as inactive toward these stimuli altogether.
View Article and Find Full Text PDFInherited DOCK2 Deficiency in Patients with Early-Onset Invasive Infections.
N Engl J Med
June 2015
From the Division of Immunology (K.D., J.C., S.K., M.J.M., K.C., K.F., T.A.C., R.S.G., L.D.N.) and Manton Center for Orphan Disease Research (L.D.N.), Boston Children's Hospital, and Department of Molecular Biology, Massachusetts General Hospital (T.K.O.), Boston, Harvard Stem Cell Institute, Harvard University, Cambridge (L.D.N.), and Department of Pediatrics, University of Massachusetts Medical School, Worcester (A.M.C.) - all in Massachusetts; CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences (C.D.C., I.B., N.K.S., M.S., C.B., K.B.), Department of Pediatrics and Adolescent Medicine, Medical University of Vienna (K.B.), and CeRUD Vienna Center for Rare and Undiagnosed Diseases (K.B.) - all in Vienna; St. Giles Laboratory of Human Genetics of Infectious Disease, Rockefeller Branch, Rockefeller University (S.-Y.Z., M.A., S.O., B.B., Y.I., L.A., J.-L.C.), and Institute for Genomic Medicine, Columbia University (S. Petrovski, D.B.G.) - both in New York; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM Unité 1163 (S.-Y.Z., V.P., L.A., J.-L.C.), Paris Descartes University, Sorbonne Paris Cité, Imagine Institute (S.-Y.Z., F.R., P.L., L.A., J.-L.C.), and Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children (J.-L.C.) - all in Paris; Howard Hughes Medical Institute, Chevy Chase, MD (J.-L.C.); Department of Molecular and Translational Medicine, University of Brescia, Brescia (S. Parolini, O.P., G.T.), and Department of Experimental Medicine and Center of Excellence for Biomedical Research, University of Genoa, Genoa (A.M.) - both in Italy; Folkhälsan Institute of Genetics and Research Programs Unit, Molecular Neurology (E.H.), Institute for Molecular Medicine Finland (J.S.), Children's Hospital (M.K.), Research Programs Unit, Diabetes and Obesity Research Program (M.K.), and Folkhälsan Research Center (M.K.), University of Helsinki and Helsinki University Central Hospital, Helsinki, Tampere Center
Background Combined immunodeficiencies are marked by inborn errors of T-cell immunity in which the T cells that are present are quantitatively or functionally deficient. Impaired humoral immunity is also common. Patients have severe infections, autoimmunity, or both.
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