Peter Murray

Summary

Affiliation: St. Jude Children's Research Hospital
Country: USA

Publications

  1. pmc Arginase-1-expressing macrophages suppress Th2 cytokine-driven inflammation and fibrosis
    John T Pesce
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA
    PLoS Pathog 5:e1000371. 2009
  2. doi request reprint Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways
    Peter J Murray
    Department of Infectious Diseases and Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee, USA
    Nat Immunol 13:916-24. 2012
  3. pmc Protective and pathogenic functions of macrophage subsets
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA
    Nat Rev Immunol 11:723-37. 2011
  4. ncbi request reprint Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Curr Opin Pharmacol 6:379-86. 2006
  5. pmc The primary mechanism of the IL-10-regulated antiinflammatory response is to selectively inhibit transcription
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 102:8686-91. 2005
  6. ncbi request reprint STAT3-mediated anti-inflammatory signalling
    P J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Biochem Soc Trans 34:1028-31. 2006
  7. ncbi request reprint The JAK-STAT signaling pathway: input and output integration
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38104, USA
    J Immunol 178:2623-9. 2007
  8. pmc Obstacles and opportunities for understanding macrophage polarization
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Pl, Memphis, TN 38105, USA
    J Leukoc Biol 89:557-63. 2011
  9. ncbi request reprint Gut Nod2 calls the bone marrow for monocyte reinforcements
    Peter J Murray
    Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Immunity 34:693-5. 2011
  10. pmc Macrophages as a battleground for toxoplasma pathogenesis
    Peter J Murray
    Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Cell Host Microbe 9:445-7. 2011

Research Grants

Collaborators

Detail Information

Publications51

  1. pmc Arginase-1-expressing macrophages suppress Th2 cytokine-driven inflammation and fibrosis
    John T Pesce
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA
    PLoS Pathog 5:e1000371. 2009
    ....
  2. doi request reprint Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways
    Peter J Murray
    Department of Infectious Diseases and Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee, USA
    Nat Immunol 13:916-24. 2012
    ....
  3. pmc Protective and pathogenic functions of macrophage subsets
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA
    Nat Rev Immunol 11:723-37. 2011
    ..Finally, we briefly discuss the characterization of macrophage heterogeneity in humans...
  4. ncbi request reprint Understanding and exploiting the endogenous interleukin-10/STAT3-mediated anti-inflammatory response
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Curr Opin Pharmacol 6:379-86. 2006
    ..Nevertheless, the signaling pathway used by the IL-10 receptor to generate the anti-inflammatory response is only beginning to be understood and could be a way to regulate inflammation by pharmacological agents...
  5. pmc The primary mechanism of the IL-10-regulated antiinflammatory response is to selectively inhibit transcription
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Proc Natl Acad Sci U S A 102:8686-91. 2005
    ....
  6. ncbi request reprint STAT3-mediated anti-inflammatory signalling
    P J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Biochem Soc Trans 34:1028-31. 2006
    ..Understanding IL-10 signalling should be a gateway to the development of broadly acting anti-inflammatory agents...
  7. ncbi request reprint The JAK-STAT signaling pathway: input and output integration
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38104, USA
    J Immunol 178:2623-9. 2007
    ..New data suggests that SOCS proteins introduce additional diversity into the JAK-STAT pathway by adjusting the output of activated STATs that alters downstream gene activation...
  8. pmc Obstacles and opportunities for understanding macrophage polarization
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Pl, Memphis, TN 38105, USA
    J Leukoc Biol 89:557-63. 2011
    ..Here, we briefly summarize current features of macrophage polarization and discuss the roles of various macrophage subpopulations and macrophage-associated genes in health and disease...
  9. ncbi request reprint Gut Nod2 calls the bone marrow for monocyte reinforcements
    Peter J Murray
    Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Immunity 34:693-5. 2011
    ..In this issue of Immunity, Kim et al. (2011) demonstrate that Nod2 is responsible for regulating monocyte-attracting chemokines to the inflamed gut...
  10. pmc Macrophages as a battleground for toxoplasma pathogenesis
    Peter J Murray
    Departments of Infectious Diseases and Immunology, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Cell Host Microbe 9:445-7. 2011
    ..The results suggest that T. gondii and the ROP kinases can be used to probe immune signaling pathways...
  11. ncbi request reprint NOD proteins: an intracellular pathogen-recognition system or signal transduction modifiers?
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Curr Opin Immunol 17:352-8. 2005
    ..However, the idea of an intracellular system that specifically recognizes bacterial cell components is controversial and alternative functions of NODs are possible including regulating signal transduction systems...
  12. pmc Increased antimycobacterial immunity in interleukin-10-deficient mice
    P J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105 2794, USA
    Infect Immun 67:3087-95. 1999
    ....
  13. ncbi request reprint Defining the requirements for immunological control of mycobacterial infections
    P J Murray
    Dept of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Trends Microbiol 7:366-72. 1999
    ..Latency - the seemingly quiescent phase of bacterial persistence - is the central problem in controlling tuberculosis and will be the next frontier of research...
  14. pmc Role of nod2 in the response of macrophages to toll-like receptor agonists
    Anne Laure Pauleau
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Mol Cell Biol 23:7531-9. 2003
    ..These results argue that Nod2 does not play an essential, nonredundant role in the response of macrophages to bacterial products but rather plays unexpected roles in regulating systemic responses to pathogens...
  15. ncbi request reprint Re-examination of the role of suppressor of cytokine signaling 1 (SOCS1) in the regulation of toll-like receptor signaling
    Sebastien Gingras
    Howard Hughes Medical Institute, Department of Biochemistry, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    J Biol Chem 279:54702-7. 2004
    ..We conclude that previous reports linking SOCS1 to TLR signaling are most likely due to effects on IFN-alpha/beta receptor signaling...
  16. ncbi request reprint SOCS3 regulates the plasticity of gp130 signaling
    Roland Lang
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    Nat Immunol 4:546-50. 2003
    ..Thus, SOCS3 functions to control the quality of the response to IL-6 and prevents the activation of an IFN-induced program of gene expression...
  17. ncbi request reprint Shaping gene expression in activated and resting primary macrophages by IL-10
    Roland Lang
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38015, USA
    J Immunol 169:2253-63. 2002
    ..For all genes examined, the effects of IL-10 were determined to be STAT3-dependent. These results suggest that IL-10 regulates STAT3-dependent pathways that selectively target a broad component of LPS-induced genes at the mRNA level...
  18. doi request reprint The TLR2-MyD88-NOD2-RIPK2 signalling axis regulates a balanced pro-inflammatory and IL-10-mediated anti-inflammatory cytokine response to Gram-positive cell walls
    Lilian O Moreira
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    Cell Microbiol 10:2067-77. 2008
    ....
  19. pmc beta-Arrestin 1 participates in platelet-activating factor receptor-mediated endocytosis of Streptococcus pneumoniae
    Jana N Radin
    Department of Infectious Diseases, St Jude Children s Research Hospital, Mailstop 320 IRC 8057, 332 N Lauderdale Rd, Memphis, TN 38105, USA
    Infect Immun 73:7827-35. 2005
    ..Overexpression of beta-arrestin in endothelial cells decreased colocalization with Rab7. We conclude that the association of beta-arrestin with the PAFr contributes to successful translocation of pneumococci...
  20. pmc Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling
    Joseph E Qualls
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    Sci Signal 3:ra62. 2010
    ....
  21. pmc The platelet activating factor receptor is not required for exacerbation of bacterial pneumonia following influenza
    Jonathan A McCullers
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38105 2794, USA
    Scand J Infect Dis 40:11-7. 2008
    ....
  22. ncbi request reprint Platelet-activating factor receptor and innate immunity: uptake of gram-positive bacterial cell wall into host cells and cell-specific pathophysiology
    Sophie Fillon
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA
    J Immunol 177:6182-91. 2006
    ..Thus, PAFr shepherds phosphorylcholine-containing bacterial components such as the cell wall into host cells from where the response ranges from quiescence to severe pathophysiology...
  23. ncbi request reprint General nature of the STAT3-activated anti-inflammatory response
    Karim C El Kasmi
    Department of Infectious Diseases, St Jude s Children s Research Hospital, Memphis, TN 38105, USA
    J Immunol 177:7880-8. 2006
    ..We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R...
  24. pmc LAG-3 regulates plasmacytoid dendritic cell homeostasis
    Creg J Workman
    Department of Immunology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
    J Immunol 182:1885-91. 2009
    ..Collectively, our data suggests that LAG-3 plays an important but selective cell intrinsic and cell extrinsic role in pDC biology, and may serve as a key functional marker for their study...
  25. ncbi request reprint WASP- mice exhibit defective immune responses to influenza A virus, Streptococcus pneumoniae, and Mycobacterium bovis BCG
    Samita Andreansky
    Department of Immunology, St Jude Children s Hospital, Memphis, TN 38104, USA
    Exp Hematol 33:443-51. 2005
    ..To quantify the immune response of WASP- mice to three different pathogens: influenza A virus, Streptococcus pneumoniae, and Mycobacterium bovis...
  26. ncbi request reprint Cutting edge: A transcriptional repressor and corepressor induced by the STAT3-regulated anti-inflammatory signaling pathway
    Karim C El Kasmi
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    J Immunol 179:7215-9. 2007
    ..Collectively our data suggest that ETV3 and SBNO2 are components of the pathways that contribute to the downstream anti-inflammatory effects of IL-10...
  27. pmc Toll-like receptor-induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens
    Karim C El Kasmi
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, Tennessee 38015, USA
    Nat Immunol 9:1399-406. 2008
    ..Specific elimination of Arg1 in macrophages favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection...
  28. pmc Conditional knockout mice reveal distinct functions for the global transcriptional coactivators CBP and p300 in T-cell development
    Lawryn H Kasper
    Department of Biochemistry, St Jude Children s Research Hospital, 332 N Lauderdale, Memphis, TN 38105, USA
    Mol Cell Biol 26:789-809. 2006
    ..Thus, CBP and p300 each supply a surprising degree of redundant coactivation capacity in T cells and macrophages, although each gene has also unique properties in thymocyte development...
  29. ncbi request reprint Autocrine deactivation of macrophages in transgenic mice constitutively overexpressing IL-10 under control of the human CD68 promoter
    Roland Lang
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN 38105, USA
    J Immunol 168:3402-11. 2002
    ....
  30. pmc Cell wall-mediated neuronal damage in early sepsis
    Carlos J Orihuela
    Infectious Diseases, St Jude Children s Research Hospital, Mailstop 320 IRC 8057, 332 N Lauderdale Rd, Memphis, TN 38105, USA
    Infect Immun 74:3783-9. 2006
    ..Thus, cell wall drives SAND through IL-10-repressible inflammatory events. Treatment with CDP-choline ameliorated SAND, suggesting that it may be an effective adjunctive therapy to increase survival and reduce organ damage in sepsis...
  31. ncbi request reprint Enhancer-mediated control of macrophage-specific arginase I expression
    Anne Laure Pauleau
    Department of Infectious Diseases, St Jude Children s Research Hospital, 332 North Lauderdale, Memphis, TN 38105, USA
    J Immunol 172:7565-73. 2004
    ..Identification of a powerful extrahepatic regulatory enhancer for arginase I provides potential to manipulate arginase I activity in immune cells while sparing liver urea cycle function...
  32. pmc Modulation of adaptive immunity by different adjuvant-antigen combinations in mice lacking Nod2
    Lilian O Moreira
    Department of Infectious Diseases, St Jude Children s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA
    Vaccine 26:5808-13. 2008
    ..Collectively, our results argue that oil emulsions deserve greater attention for their immunostimulatory properties...
  33. pmc Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival
    Mohamed Lamkanfi
    Department of Immunology, St Jude Children s Research Hospital, Memphis, TN 38105 2794, USA
    Blood 113:2742-5. 2009
    ..These results reveal for the first time a nonredundant role for caspase-7 in vivo and identify caspase-7 inhibition as a component of the mechanism by which caspase inhibitors protect from endotoxin-induced mortality...
  34. ncbi request reprint Nucleotide binding oligomerization domain 2 deficiency leads to dysregulated TLR2 signaling and induction of antigen-specific colitis
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, Room 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
    Immunity 25:473-85. 2006
    ..Thus, NOD2-deficient mice become susceptible to colitis as a result of increased TLR2 responses when they have the capacity to respond to an antigen expressed by mucosal bacteria...
  35. pmc Abrogation of anti-retinal autoimmunity in IL-10 transgenic mice due to reduced T cell priming and inhibition of disease effector mechanisms
    Rajeev K Agarwal
    The Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 180:5423-9. 2008
    ....
  36. ncbi request reprint IL-10 suppresses mast cell IgE receptor expression and signaling in vitro and in vivo
    Sarah Kennedy Norton
    Department of Biology, Virginia Commonwealth University, Richmond, VA 23284, USA
    J Immunol 180:2848-54. 2008
    ..IL-10 may hence serve as a mediator of mast cell homeostasis, preventing excessive activation and the development of chronic inflammation...
  37. pmc Persistent Coxiella burnetii infection in mice overexpressing IL-10: an efficient model for chronic Q fever pathogenesis
    Soraya Meghari
    Unite des Rickettsies, CNRS UMR 6020, Institut Federatif de Recherche 48, Universite de la Mediterranee, Faculte de Medecine, Marseille, France
    PLoS Pathog 4:e23. 2008
    ..To our knowledge, this is the first efficient model for chronic Q fever pathogenesis...
  38. ncbi request reprint IL-10-independent STAT3 activation by Toxoplasma gondii mediates suppression of IL-12 and TNF-alpha in host macrophages
    Barbara A Butcher
    Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA
    J Immunol 174:3148-52. 2005
    ..gondii exploits host STAT3 to prevent LPS-triggered IL-12 and TNF-alpha production, revealing for the first time a molecular mechanism underlying the parasite's suppressive effect on macrophage proinflammatory cytokine production...
  39. ncbi request reprint Control of dual-specificity phosphatase-1 expression in activated macrophages by IL-10
    Michael Hammer
    Institute of Medical Microbiology, Immunology and Hygiene, Technical University Munich, Munich, Germany
    Eur J Immunol 35:2991-3001. 2005
    ..Thus, these data suggest an operational link between IL-10 and inhibition of p38 MAPK via sustained expression of DUSP1...
  40. ncbi request reprint Hypervirulent M. tuberculosis W/Beijing strains upregulate type I IFNs and increase expression of negative regulators of the Jak-Stat pathway
    Claudia Manca
    Laboratory of Mycobacterial Immunity and Pathogenesis, Public Health Research Institute, International Center for Public Health, 225 Warren Street, Newark, NJ 07103 3535, USA
    J Interferon Cytokine Res 25:694-701. 2005
    ..Taken together, these results suggest that increased type I IFNs may be deleterious for survival of M. tuberculosis-infected mice in association with reduced Th1 immunity...
  41. ncbi request reprint Induction of suppressor of cytokine signaling-1 by Toxoplasma gondii contributes to immune evasion in macrophages by blocking IFN-gamma signaling
    Stefan Zimmermann
    Institute of Medical Microbiology and Hygiene, Philipps University, Marburg, Germany
    J Immunol 176:1840-7. 2006
    ..gondii on IFN-gamma were diminished in macrophages from SOCS-1-/- mice. The results suggest that induction of SOCS proteins within phagocytes due to infection with T. gondii contributes to the parasite's immune evasion strategies...
  42. pmc Nucleotide-binding oligomerization domain protein 2-deficient mice control infection with Mycobacterium tuberculosis
    Sheetal Gandotra
    Department of Microbiology and Immunology, Weill Cornell Medical College, Box 62, 1300 York Avenue, New York, NY 10021, USA
    Infect Immun 75:5127-34. 2007
    ..tuberculosis infection. Thus, NOD2 appears to participate in the recognition of M. tuberculosis by antigen-presenting cells in vitro yet is dispensable for the control of the pathogen during in vivo infection...
  43. ncbi request reprint IFN regulatory factor 3-dependent induction of type I IFNs by intracellular bacteria is mediated by a TLR- and Nod2-independent mechanism
    Silvia Stockinger
    Max F Perutz Laboratories, University Department at the Vienna Biocenter, Department of Microbiology and Genetics, University of Vienna, Austria
    J Immunol 173:7416-25. 2004
    ..monocytogenes stimulates a novel TLR- and Nod2-independent pathway to target IRF3 and the type I IFN genes...
  44. pmc Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation
    Divya Vats
    Division of Endocrinology, Metabolism and Gerontology, Department of Medicine and Graduate Program in Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
    Cell Metab 4:13-24. 2006
    ....
  45. ncbi request reprint Interleukin-10 induces apoptosis in developing mast cells and macrophages
    Daniel P Bailey
    Department of Biology, Virginia Commonwealth University, Richmond, 23284 2012, USA
    J Leukoc Biol 80:581-9. 2006
    ..The ability of IL-10 to inhibit survival could support immune homeostasis by dampening inflammatory responses and preventing chronic inflammation...
  46. ncbi request reprint NOD2 is a negative regulator of Toll-like receptor 2-mediated T helper type 1 responses
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 Room 11N238, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Immunol 5:800-8. 2004
    ..Thus, CARD15 mutations may lead to disease by causing excessive T(H)1 responses...
  47. pmc Cytokine signaling modules in inflammatory responses
    JOHN J O'SHEA
    Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20852, USA
    Immunity 28:477-87. 2008
    ....
  48. pmc Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitis
    Tomohiro Watanabe
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892, USA
    J Clin Invest 118:545-59. 2008
    ....
  49. pmc STAT3 governs distinct pathways in emergency granulopoiesis and mature neutrophils
    Athanasia D Panopoulos
    Department of Immunology, The University of Texas M D Anderson Cancer Center, PO Box 301402, Unit 902, Houston, TX 77030 1903, USA
    Blood 108:3682-90. 2006
    ..Our results demonstrate the existence of distinct STAT3 target pathways in neutrophils required for granulopoiesis and innate immunity...
  50. ncbi request reprint Targeting vector construction by yeast artificial chromosome modification
    Peter J Murray
    Department of Infectious Diseases, St Jude Children s Research Hospital, Memphis, TN, USA
    Methods Mol Biol 349:127-37. 2006
    ..This chapter describes a simple procedure where YACs can be modified to produce targeting vectors of various sizes...
  51. ncbi request reprint Signalling pathways and molecular interactions of NOD1 and NOD2
    Warren Strober
    Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10 CRC, 5W3940, 10 Center Drive, Bethesda, Maryland 20892, USA
    Nat Rev Immunol 6:9-20. 2006
    ....

Research Grants5

  1. Role of SOCS proteins in host-pathogen responses
    Peter Murray; Fiscal Year: 2003
    ..PERFORMANCE SITE (S) (organization, city, state) St. Jude Children's Research Hospital, Memphis, TN . ..
  2. Role of Macrophage Arginase in Anti-Bacterial Immunity
    Peter Murray; Fiscal Year: 2009
    ..The outcomes of the proposed studies will reveal new elements of Arg I function and provide rationale for approaching Arg I as a target in inflammatory diseases. ..