Research Topics
Genomes and Genes
| David H McDermottSummaryAffiliation: National Institutes of Health Country: USA Publications
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Detail Information
Publications
AMD3100 is a potent antagonist at CXCR4(R334X) , a hyperfunctional mutant chemokine receptor and cause of WHIM syndromeDavid H McDermott
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
J Cell Mol Med 15:2071-81. 2011..Together, our data provide further evidence that CXCR4(R334X) is a gain-of-function mutation, and support clinical evaluation of AMD3100 as mechanism-based treatment in patients with WHIM syndrome...
CCL2 polymorphisms are associated with serum monocyte chemoattractant protein-1 levels and myocardial infarction in the Framingham Heart StudyDavid H McDermott
National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1886, USA
Circulation 112:1113-20. 2005..Monocyte chemoattractant protein-1 (MCP-1) is a chemokine strongly implicated in promoting atherosclerosis in animal models, but human genetic evidence is contradictory...- Severe congenital neutropenia resulting from G6PC3 deficiency with increased neutrophil CXCR4 expression and myelokathexisDavid H McDermott
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Blood 116:2793-802. 2010..Thus, myelokathexis associated with abnormally high neutrophil CXCR4 expression may contribute to neutropenia in G6PC3 deficiency and responds well to granulocyte colony-stimulating factor... - CCR5 deficiency is a risk factor for early clinical manifestations of West Nile virus infection but not for viral transmissionJean K Lim
Molecular Signaling Section, Laboratory of Molecular Immunology, Laboratory of Cellular and Molecular Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA
J Infect Dis 201:178-85. 2010.... - Lack of glucose recycling between endoplasmic reticulum and cytoplasm underlies cellular dysfunction in glucose-6-phosphatase-beta-deficient neutrophils in a congenital neutropenia syndromeHyun Sik Jun
Section on Cellular Differentiation, Program on Developmental Endocrinology and Genetics, National Institute of Child Health and Human Development, National Institutes of Health NIH, Bethesda, MD, USA
Blood 116:2783-92. 2010..The results establish that in nonapoptotic neutrophils, G6Pase-β is essential for normal energy homeostasis. A G6Pase-β deficiency prevents recycling of ER glucose to the cytoplasm, leading to neutrophil dysfunction... - WHIM syndrome caused by a single amino acid substitution in the carboxy-tail of chemokine receptor CXCR4Qian Liu
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Blood 120:181-9. 2012..Therefore, in addition to truncating mutations in the C-terminal domain of CXCR4, WHIM syndrome may be caused by a single charge-changing amino acid substitution in this domain, E343K, that results in increased receptor signaling... - The CXCR4 antagonist plerixafor corrects panleukopenia in patients with WHIM syndromeDavid H McDermott
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Blood 118:4957-62. 2011..This study is registered at http://www.clinicaltrials.gov as NCT00967785... 
Genetic deficiency of chemokine receptor CCR5 is a strong risk factor for symptomatic West Nile virus infection: a meta-analysis of 4 cohorts in the US epidemicJean K Lim
Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Infect Dis 197:262-5. 2008..1 [95% CI, 0.9-11.2] [P= .06]). A meta-analysis of all 4 cohorts showed an OR of 4.2 (95% CI, 2.1-8.3 [P= .0001]). Thus, CCR5 deficiency is a strong and consistent risk factor for symptomatic WNV infection in the United States...- Genetic variation in OAS1 is a risk factor for initial infection with West Nile virus in manJean K Lim
Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA
PLoS Pathog 5:e1000321. 2009..0001). Together, these data identify OAS1 SNP rs10774671 as a host genetic risk factor for initial infection with WNV in humans... - CCR5: no longer a "good for nothing" gene--chemokine control of West Nile virus infectionJean K Lim
Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Trends Immunol 27:308-12. 2006..Although CCR5 might be a logical target for new drug development in HIV/AIDS, the benefits of blocking CCR5 could carry the cost of an increased risk of WNV disease in co-infected patients... - Interleukin (IL)-15 and IL-2 reciprocally regulate expression of the chemokine receptor CX3CR1 through selective NFAT1- and NFAT2-dependent mechanismsJana Barlic
Molecular Signaling Section, Laboratory of Host Defenses, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
J Biol Chem 279:48520-34. 2004..We propose that expression of CX3CR1 and possibly other immunoregulatory genes may be determined in part by the balance of NFAT1 and NFAT2 activity in leukocytes... - CCR5 deficiency increases risk of symptomatic West Nile virus infectionWilliam G Glass
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Exp Med 203:35-40. 2006..03). We conclude that CCR5 mediates resistance to symptomatic WNV infection. Because CCR5 is also the major HIV coreceptor, these findings have important implications for the safety of CCR5-blocking agents under development for HIV/AIDS... - Complete genome sequence of a tenth human polyomavirusChristopher B Buck
NCI, Bethesda, Maryland, USA
J Virol 86:10887. 2012.... - Donor and recipient chemokine receptor CCR5 genotype is associated with survival after bone marrow transplantationDavid H McDermott
Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
Blood 115:2311-8. 2010..This finding suggests that donor and/or recipient CCR5 genotypes may be associated with HSCT outcome and suggests new diagnostic and therapeutic strategies for optimizing therapy... - Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient miceWuzhou Wan
Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
Circ Res 109:374-81. 2011..Recent evidence suggests that both CCR6 and its ligand CCL20 are also present in human atheroma; however, their functional roles in atherogenesis remain undefined... - Chemokine receptor mutant CX3CR1-M280 has impaired adhesive function and correlates with protection from cardiovascular disease in humansDavid H McDermott
Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases/NIH, Building 10, 9000 Rockville Pike, Bethesda, MD 20892-1886, USA
J Clin Invest 111:1241-50. 2003..Moreover, they suggest that CX3CR1-M280 is a genetic risk factor for CVD... - Associations of chemokine system polymorphisms with clinical outcomes and treatment responses of chronic hepatitis CKittichai Promrat
The Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
Gastroenterology 124:352-60. 2003..The roles of other disease-associated chemokine system polymorphisms have not been evaluated in hepatitis C virus infection... - Role for CCR5Delta32 protein in resistance to R5, R5X4, and X4 human immunodeficiency virus type 1 in primary CD4+ cellsLokesh Agrawal
Department of Microbiology and Immunology and Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
J Virol 78:2277-87. 2004.... - Chemokine receptor polymorphism and risk of acute rejection in human renal transplantationReza Abdi
Renal Division, Brigham and Women s Hospital, Boston, Massachesetts, USA
J Am Soc Nephrol 13:754-8. 2002..20; P = 0.032) and homozygosity for the 59029-A allele (OR, 0.26; P = 0.027). It was concluded that the risk of acute rejection in renal transplantation is associated with genetic variation in the chemokine receptors CCR2 and CCR5... - Role of beta3 integrin in acute renal allograft rejection in humansArun Chandrakantan
Division of Nephrology, University of Alabama at Birmingham, Birmingham, Alabama, USA
Clin J Am Soc Nephrol 2:1268-73. 2007..Beta3 Integrin may play a role in the process of acute rejection by increasing leukocyte adhesion to the endothelium, cytotoxic T lymphocyte activation, and platelet aggregation... - Assessment of cumulative evidence on genetic associations: interim guidelinesJohn P A Ioannidis
Clinical and Molecular Epidemiology Unit, University of Ioannina School of Medicine, Ioannina 45110, Greece
Int J Epidemiol 37:120-32. 2008..Future empirical research and consensus development are needed to develop an integrated model for combining epidemiological and biological evidence in the rapidly evolving field of investigation of genetic factors...