Philip M. Murphy, M.D.Building 10, Room 11N11110 Center DriveBethesda, MD 20892-1886Phone: 301-496-8616Fax: firstname.lastname@example.org
Chief, Laboratory of Molecular ImmunologyChief, Molecular Signaling Section, LMI
This laboratory studies G protein-coupled receptors of the immune system. These include a large family of chemokine receptors and a smaller group of classical chemoattractant receptors, which together differentially regulate specific leukocyte trafficking in support of innate and adaptive immune responses.
The goal of the lab is to delineate the precise mechanisms by which the receptors relay chemotactic signals to cells and to identify their exact physiologic roles both in immunoregulation and in immunologically mediated disease. The approaches used are to isolate specific chemoattractant receptors by molecular cloning, to examine their signal transduction properties both in model cell systems and in primary cells, and to study their biology in mouse models and, where possible, in patients through direct clinical research.
Further, the lab has a program in human immunogenomics in which genetic polymorphisms discovered in candidate chemoattractant or chemoattractant receptor genes are checked for effects on biochemical function and for associations with specific diseases. Major discoveries include the following:
There are projects ongoing in the lab extending each of these observations.
Dr. Murphy obtained an A.B. from Princeton University in 1975 and an M.D. from Cornell University Medical College in 1981. He trained in internal medicine at New York University from 1981 to 1985, serving as chief resident from 1984 to 1985, and in infectious diseases at NIAID from 1985 to 1988.
He began his research career as a medical staff fellow in the Bacterial Diseases Section of the NIAID Laboratory of Clinical Investigation in 1986 and was promoted to senior investigator with tenure in the Laboratory of Host Defenses (LHD) in 1992. In 1998, he was promoted to the Senior Biomedical Research Service and named chief of the LHD Molecular Signaling Section.
In 2003, Dr. Murphy’s research group was reorganized as part of the new Laboratory of Molecular Immunology, where he served first as acting chief from 2003 to 2006 and then as chief from 2006 to the present. Dr. Murphy’s research interests include immunoregulation by chemokines and related chemoattractants.
NIH Merit Award (1992); NIH Director's Award (1994, 1996); NIH Senior Biomedical Research Service (1998); American Society for Clinical Investigation (1992); Association of American Physicians (1997); the Henry Kunkel Society (2006); NIAID Merit Award (2009); NIAID Mentor of the Year Award (2010)
Jenny DworzakJi-Liang GaoZhanzhuo LiJoy LiuAna MarinoDavid McDermottErich SchneiderAurelie TomczakDaniel VelezJoe WanDon WeaverSunny Yung
Wan W, Lim JK, Lionakis MS, Rivollier A, McDermott DH, Kelsall BL, Farber JM, Murphy PM. Genetic deletion of chemokine receptor Ccr6 decreases atherogenesis in ApoE-deficient mice. Circ Res. 2011 Aug 5;109(4):374-81.
Yung SC, Parenti D, Murphy PM. Host chemokines bind to Staphylococcus aureus and stimulate protein A release. J Biol Chem. 2011 Feb 18;286(7):5069-77.
Lim JK, Obara CJ, Rivollier A, Pletnev AG, Kelsall BL, Murphy PM. Chemokine receptor CCR2 is critical for monocyte accumulation and survival in West Nile virus encephalitis. J Immunol. 2011 Jan 1;186(1):471-8.
Lionakis MS, Lim JK, Lee CC, Murphy PM. Organ-specific innate immune responses in a mouse model of invasive candidiasis. J Innate Immun. 2011;3(2):180-99.
McDermott DH, De Ravin SS, Jun HS, Liu Q, Priel DA, Noel P, Takemoto CM, Ojode T, Paul SM, Dunsmore KP, Hilligoss D, Marquesen M, Ulrick J, Kuhns DB, Chou JY, Malech HL, Murphy PM. Severe congenital neutropenia resulting from G6PC3 deficiency with increased neutrophil CXCR4 expression and myelokathexis. Blood. 2010 Oct 14;116(15):2793-802.
Barlic J, Zhu W, Murphy PM. Atherogenic lipids induce high-density lipoprotein uptake and cholesterol efflux in human macrophages by up-regulating transmembrane chemokine CXCL16 without engaging CXCL16-dependent cell adhesion. J Immunol. 2009 Jun 15;182(12):7928-36.
Visit PubMed for a complete publication list.
Genetic Factors in Atherosclerosis, #00-I-0143
A Phase I Study of Mozobil in the Treatment of Patients with WHIMS, #09-I-0200
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Last Updated March 26, 2013