Peter J Murray

Summary

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

Publications

  1. Kamei A, Gao G, Neale G, Loh L, Vogel P, Thomas P, et al. Exogenous remodeling of lung resident macrophages protects against infectious consequences of bone marrow-suppressive chemotherapy. Proc Natl Acad Sci U S A. 2016;113:E6153-E6161 pubmed
    ..Thus, induction of ViMs by tissue macrophage remodeling may become a framework for new strategies to activate immune-mediated reserves against infection in immunocompromised hosts. ..
  2. Murray P. Obesity corrupts myelopoiesis. Cell Metab. 2014;19:735-6 pubmed publisher
    ..Nagareddy et al. (2014) show that adipose cells locally activate IL-1? in macrophages in part through the alarmin S100A8/A9, which stimulates bone marrow myelopoiesis to perpetuate nonresolving inflammation. ..
  3. Murray P. Macrophages as a battleground for toxoplasma pathogenesis. Cell Host Microbe. 2011;9:445-7 pubmed publisher
    ..The results suggest that T. gondii and the ROP kinases can be used to probe immune signaling pathways. ..
  4. Kratochvill F, Neale G, Haverkamp J, Van De Velde L, Smith A, Kawauchi D, et al. TNF Counterbalances the Emergence of M2 Tumor Macrophages. Cell Rep. 2015;12:1902-14 pubmed publisher
    ..Our results show macrophage polarization in cancer is dynamic and dependent on the balance between TNF and IL-13, thus providing a strategy for manipulating TAMs. ..
  5. Qualls J, Murray P. Immunometabolism within the tuberculosis granuloma: amino acids, hypoxia, and cellular respiration. Semin Immunopathol. 2016;38:139-52 pubmed publisher
    ..While elimination of the TB bacilli is often the goal of any anti-TB therapy, host-directed approaches must also account for the possibility of immunopathologic damage to the lung. ..
  6. Murray P. Macrophage Polarization. Annu Rev Physiol. 2017;79:541-566 pubmed publisher
    ..Here, I assess the current state of knowledge about macrophage polarization and enumerate the major questions about how activated macrophages regulate the physiology of normal and damaged tissues. ..
  7. Murray P, Wynn T. Protective and pathogenic functions of macrophage subsets. Nat Rev Immunol. 2011;11:723-37 pubmed publisher
    ..Finally, we briefly discuss the characterization of macrophage heterogeneity in humans. ..
  8. Murray P, Smale S. Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways. Nat Immunol. 2012;13:916-24 pubmed publisher
  9. Haverkamp J, Smith A, Weinlich R, Dillon C, Qualls J, Neale G, et al. Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways. Immunity. 2014;41:947-59 pubmed publisher
    ..Thus, death pathway modulation defines the development, survival, and function of myeloid suppressor cells. ..

More Information

Publications18

  1. Marigo I, Zilio S, Desantis G, Mlecnik B, Agnellini A, Ugel S, et al. T Cell Cancer Therapy Requires CD40-CD40L Activation of Tumor Necrosis Factor and Inducible Nitric-Oxide-Synthase-Producing Dendritic Cells. Cancer Cell. 2016;30:377-390 pubmed publisher
    ..Our results identify a network of pro-tumor factors that can be targeted to boost cancer immunotherapies. ..
  2. Van De Velde L, Subramanian C, Smith A, Barron L, Qualls J, Neale G, et al. T Cells Encountering Myeloid Cells Programmed for Amino Acid-dependent Immunosuppression Use Rictor/mTORC2 Protein for Proliferative Checkpoint Decisions. J Biol Chem. 2017;292:15-30 pubmed publisher
    ..Arginine deprivation-induced cell cycle arrest was mediated in part by Rictor/mTORC2, providing evidence that this nutrient recognition pathway is a central component of how T cells measure environmental arginine. ..
  3. Kratochvill F, Gratz N, Qualls J, Van De Velde L, Chi H, Kovarik P, et al. Tristetraprolin Limits Inflammatory Cytokine Production in Tumor-Associated Macrophages in an mRNA Decay-Independent Manner. Cancer Res. 2015;75:3054-64 pubmed publisher
    ..Manipulation of the p38α-TTP axis in macrophages has significant effects on the growth of tumors and therefore represents a means to manipulate inflammation in the tumor microenvironment. ..
  4. Murray P, Allen J, Biswas S, Fisher E, Gilroy D, Goerdt S, et al. Macrophage activation and polarization: nomenclature and experimental guidelines. Immunity. 2014;41:14-20 pubmed publisher
    ..Collectively, we propose a common framework for macrophage-activation nomenclature. ..
  5. Van De Velde L, Gingras S, Pelletier S, Murray P. Issues with the Specificity of Immunological Reagents for Murine IDO1. Cell Metab. 2016;23:389-90 pubmed publisher
  6. Van De Velde L, Murray P. Proliferating Helper T Cells Require Rictor/mTORC2 Complex to Integrate Signals from Limiting Environmental Amino Acids. J Biol Chem. 2016;291:25815-25822 pubmed
    ..Our data suggest that Rictor/mTORC2 controls an amino acid-sensitive checkpoint that allows T cells to determine whether the microenvironment contains sufficient resources for daughter cell generation. ..
  7. request reprint
    Murray P. The JAK-STAT signaling pathway: input and output integration. J Immunol. 2007;178:2623-9 pubmed
    ..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. Van De Velde L, Guo X, Barbaric L, Smith A, Oguin T, Thomas P, et al. Stress Kinase GCN2 Controls the Proliferative Fitness and Trafficking of Cytotoxic T Cells Independent of Environmental Amino Acid Sensing. Cell Rep. 2016;17:2247-2258 pubmed publisher
    ..Thus, GCN2 is required for normal cytotoxic T cell function. ..
  9. Murray P. The primary mechanism of the IL-10-regulated antiinflammatory response is to selectively inhibit transcription. Proc Natl Acad Sci U S A. 2005;102:8686-91 pubmed