Peter J. Murray, PhD

Peter J. Murray, PhD

Associate Member, St. Jude Faculty

Departments

Infectious Diseases
Immunology

Contact Information

Peter Murray, PhD
Infectious Diseases
MS320, Room E8078
St. Jude Children's Research Hospital
262 Danny Thomas Place
Memphis, TN 38105-3678
Email: peter.murray@stjude.org
Phone: (901) 595-3219
FAX: (901) 595-3099

Education

PhD - University of Melbourne/Walter & Eliza Hall Institute of Medical Research (1991)


Research Interests

The innate immune response has two major functions: the early recognition and response to pathogen invaders of all varieties and the subsequent and ongoing optimization of the adaptive (T and B cell-mediated) immune response that is ultimately responsible for the elimination of pathogens and the development of memory. The innate immune response is subject to an extraordinarily complex series of regulatory events to maximize anti-pathogen responses but also to constrain the deleterious effects of innate immune response-driven inflammation. We study the regulatory events that control the innate immune response. Specifically, we focus on macrophage activation and deactivation because these cells are principally responsible for driving inflammation in a plenitude of infections and other chronic and acute diseases.

Additional research information


Selected Publications

Kobayashi T, Russo SM, Matsuoka K, Nochi T, Maharshak N, Borst LB, Hostager B, Garcia-Martinez JV, Rothman PB, Kashiwada M, Sheikh S, Murray PJ, Plevy SE. NFIL3 deficient mice develop IL-12/23 driven spontaneous colitis. J. Immunol 192: 1918-1927, 2014.

Murray PJ, Smale ST. Restraint of inflammatory signaling by interdependent strata of negative regulatory pathways. Nat Immunol 13(10):916-24, 2012.

Qualls JE, Subramanian C, Rafi W, Smith AM, Balouzian L, Defreitas AA, Shirey KA, Reutterer B, Kernbauer E, Stockinger S, Decker T, Miyairi I, Vogel SN, Salgame P, Rock CO, Murray PJ. Sustained generation of nitric oxide and control of mycobacterial infection requires argininosuccinate synthase 1. Cell Host Microbe 12(3):313-23, 2012.

Murray PJ, Wynn TA. Protective and pathogenic functions of macrophage subsets. Nat Rev Immunol 11(11):723-37, 2011.

Smith AM, Qualls JE, O'Brien K, Balouzian L, Johnson PF, Schultz-Cherry S, Smale ST, Murray PJ. A distal enhancer in IL12b is the target of transcriptional repression by the STAT3 pathway and requires the basic leucine zipper (B-ZIP) protein NFIL3. J Biol Chem 286(26):23582-90, 2011.

Qualls JE, Neale G, Smith AM, Koo MS, Defreitas AA, Zhang H, Kaplan G, Watowich SS, Murray PJ. Arginine usage in mycobacteria-infected macrophages depends on autocrine-paracrine cytokine signaling. Sci Signal 3(135):ra62, 2010.

Pesce JT, Cheever AW, Ramalingam TR, Wilson MS, Mentink-Kane MM, El Kasmi KC, Smith AM, Thompson RW, Murray PJ*, Wynn TA* Macrophage/neutrophil specific arginase 1 functions as a negative regulator of Th2-driven inflammation and fibrosis. PLoS Pathogens 5(4): (2009) e1000371. *Equal corresponding authors

El Kasmi KC, Qualls JE, Pesce JT, Smith AM, Thompson RW, Henao-Tamayo M, Basaraba RJ, Konig T, Schleicher U, Koo MS, Kaplan G, Fitzgerald KA, Tuomanen EI, Orme IM, Kanneganti T-D, Bogdan C, Wynn TA, Murray PJ. Toll-like receptor-induced arginase 1 thwarts effective immunity against intracellular pathogens. Nature Immunol 9:1399-1406, 2008.

O’Shea JJ, Murray PJ. Cytokine signaling modules in inflammatory responses. Immunity 28: 477-487, 2008.

El Kasmi KC, Smith AM, Neale G, Williams LM, Panopoulos A, Watowich SS, Häcker H, Foxwell BMJ, Murray PJ. A transcriptional repressor and co-repressor induced by the anti-inflammatory signaling pathway. J Immunol 179: 7215-7219, 2007.

Murray PJ. The JAK-STAT signaling pathway: Input and output integration. J Immunol 178: 2623-2629, 2007.

El Kasmi KC, Holst J, Coffre M, Mielke L, de Pauw A, Lhocine N, Smith AM, Rutschman R, Kaushal D, Shen Y, Suda T, Donnelly RP, Myers MG Jr, Alexander WS, Vignali DAA, Watowich SS, Ernst M, Hilton DJ, Murray PJ. General nature of the STAT3-activated anti-inflammatory response. J Immunol 177: 7880-7888, 2006.

Murray PJ. The primary mechanism of the IL-10-regulated anti-inflammatory response is to selectively inhibit transcription. Proc Natl Acad Sci USA 102: 8686-8691, 2005.

Gingras S, Parganas E, de Pauw A, Ihle JN, Murray PJ. Re-examination of the role of SOCS1 in the regulation of Toll-like receptor signaling. J Biol Chem 279: 54702-54707, 2004.

Pauleau A-L, Rutschman R, Lang R, Pernis A, Watowich SS, Murray PJ.  Enhancer-mediated control of macrophage-specific arginase I expression. J Immunol 172: 7565-7573, 2004.

Lang R, Pauleau A-L, Takahashi Y, Mages J, Parganas E, Ihle JN, Rutschman R, Murray PJ. SOCS3 regulates the plasticity of gp130 signaling. Nature Immunol 4: 546-550, 2003.

Lang R, Patel D, Morris J, Rutschman R, Murray PJ. Shaping gene expression in activated and resting primary macrophages by IL-10. J Immunol 169: 2253-2263, 2002.

Lang R, Rutschman R, Greaves DR, Murray PJ. Autocrine deactivation of macrophages in transgenic mice constitutively overexpressing IL-10 under control of the human CD68 promoter. J Immunol 168: 3402-3411, 2001.

Rutschman R, Lang R, Hesse M, Ihle JN, Wynn T, Murray PJ. Stat6-dependent substrate depletion regulates nitric oxide depletion. J Immunol 166: 2173-2177, 2001.

Last update: March 2014