• Publications
  • Influence
Protective and pathogenic functions of macrophage subsets
The four stages of orderly inflammation mediated by macrophages are discussed: recruitment to tissues; differentiation and activation in situ; conversion to suppressive cells; and restoration of tissue homeostasis. Expand
Macrophage activation and polarization: nomenclature and experimental guidelines.
A set of standards encompassing three principles-the source of macrophages, definition of the activators, and a consensus collection of markers to describe macrophage activation are described with the goal of unifying experimental standards for diverse experimental scenarios. Expand
Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards
The authors identify the challenges and proposed set of minimal reporting guidelines for mouse and human MDSC are a heterogeneous population expanded in cancer and other chronic inflammatory conditions. Expand
Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation.
It is shown that in response to interleukin-4, signal transducer and activator of transcription 6 (STAT6) and PPARgamma-coactivator-1 beta (PGC-1beta) induce macrophage programs for fatty acid oxidation and mitochondrial biogenesis, suggesting a potential role for metabolic therapies in treating atherogenic inflammation. Expand
The JAK-STAT Signaling Pathway: Input and Output Integration1
  • P. Murray
  • Biology, Medicine
  • The Journal of Immunology
  • 1 March 2007
This work discusses how diverse outcomes in gene expression result from regulatory events that effect the JAK1-STAT3 pathway, common to both receptors and considers how the suppressor of cytokine signaling (SOCS) proteins regulate the quality and quantity of STAT signals from cytokine receptors. Expand
NOD2 is a negative regulator of Toll-like receptor 2–mediated T helper type 1 responses
Card15 deficiency or the presence of a Crohn disease–like Card15 mutation increased Toll-like receptor 2–mediated activation of NF-κB–c-Rel, and TH1 responses were enhanced, suggesting that CARD15 mutations may lead to disease by causing excessive TH 1 responses. Expand
Macrophage Polarization.
  • P. Murray
  • Medicine
  • Annual review of physiology
  • 2017
The current state of knowledge about macrophage polarization is assessed and the major questions about how activated macrophages regulate the physiology of normal and damaged tissues are enumerated. Expand
Signalling pathways and molecular interactions of NOD1 and NOD2
This work focuses on the molecular interactions between these NOD proteins and other intracellular molecules to elucidate the mechanisms by which NOD1 and NOD2 contribute to the maintenance of mucosal homeostasis and the induction of mucosa inflammation. Expand
Shaping Gene Expression in Activated and Resting Primary Macrophages by IL-101
Results suggest that IL-10 regulates STAT3-dependent pathways that selectively target a broad component of LPS-induced genes at the mRNA level, which is consistent with previous reports on cytokine signaling-3 and IL-1 receptor antagonist. Expand
Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis
Data identify Arg1 as the essential suppressive mediator of alternatively activated macrophages (AAM) and demonstrate that Arg1-expressing macrophage function as suppressors rather than inducers of Th2-dependent inflammation and fibrosis. Expand