Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens

By K. Kasmi, J. Qualls, J. Pesce, A. Smith, Robert W. Thompson, Marcela Henao-Tamayo, R. Basaraba, Till König, U. Schleicher, Mi-Sun Koo and 8 more. Nature Immunology, 2008

649 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/489d0db21b66506c2a3e8def9b8a3f948f129725

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Citations in the corpus

Tumor-induced tolerance and immune suppression depend on the C/EBPbeta transcription factor. (2010, background): “Cg-Tg(Tek-Cre)1Ywa (Tie2 transgene abbreviated here as Tie2cre), as previously reported for other genes (El Kasmi et al., 2008).”
Arginase: an emerging key player in the mammalian immune system (2009, background): “In contrast, murine viability in the context of sepsis models (by LPS challenge or Streptococcus pneumoniae inoculation) was unaltered in the context of macrophage arginase-deficiency (El Kasmi et al., 2008).”
Alternative activation of macrophages: mechanism and functions. (2010, background): “There are obvious caveats to the use of reverse analysis alone, as required in human studies in situ: substantial species differences exist in available markers, and established markers such as Arg1 can be induced by other pathways (El Kasmi et al., 2008).”
Macrophages: Master Regulators of Inflammation and Fibrosis (2010, background): “Given the presumably important contribution of AAMw to the development of fibrosis, a great deal of recent research has sought to identify the signals that regulate their activation and recruitment to sites of inflammation, with IL4, IL-13, IL-10, granulocyte-macrophage colony-stimulating factor, IL”
Metabolism via Arginase or Nitric Oxide Synthase: Two Competing Arginine Pathways in Macrophages (2014, background): “Another layer of complexity comes into play by the demonstration of pathogen-induced toll-like receptor (TLR)-mediated induction of arginase I in murine macrophages (67, 68).”
The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation (2011, methodology): “Arg1flox/flox; Tie2Cre mice that were backcrossed to the C57BL/6 background were obtained from P. Murray (SJCRH, Memphis) (El Kasmi et al., 2008).”
Macrophage Polarization. (2017, background): “F or p er so na l u se o nl y. Table 1 (Continued ) Protein (gene)a Function Genetic lesionb Effect on polarization Reference(s) Notes IRF5 (Irf5) Transcription factor Conditional knockout (LysM-Cre) Complete knockout Loss of M1 65, 106 None TSC1 (Tsc1) Inhibitor of mTOR Conditional knockout (LysM-C”
Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis (2009, background): “Recently, we showed that Arg1-expressing macrophages also regulate type-1 responses [8].”
Microglial M1/M2 polarization and metabolic states (2016, background): “In addition, the primary ‘marker’ for M2, Arg1, is also induced in M1 macrophages and expressed in some resident and mycobacteriainfected macrophages (El Kasmi et al., 2008).”
Novel Markers to Delineate Murine M1 and M2 Macrophages (2015, background): “Arginase-1 is up-regulated not only in the expected M2 macrophages but also in M1 spectrum macrophages [30,31].”
Macrophage activation and polarization: nomenclature and experimental guidelines (2014, positive): “…has led to interpretive problems because Arg1 is also induced in M1 spectrum macrophages, expressed in some resident macrophage populations, and highly induced in mycobacteria-infected macrophages, further emphasizing the need for criteria encompassing multiple markers (El Kasmi et al., 2008).”
Macrophage phenotypes in atherosclerosis (2014, background): “In response to TLR signaling, Arg1 induction is mediated by C/EBPb in murine macrophages (96).”
INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, positive): “Importantly, although IL-4-mediated Arg1 induction in AAMs relies on STAT6 (42), Arg1 can also be induced by STAT3-dependent activation in the absence of other AAM markers after TLR stimulation or Mycobacterium tuberculosis infection, via signaling through the TLR adapter myeloid differentiation mar”
Transcriptional regulation of macrophage polarization: enabling diversity with identity (2011, background): “Both STAT6 and C/EBPβ have recently been shown to be essential for arginase 1 expression in macrophages, but in a stimulus-specific manner owing to the selective use of distinct cis -acting elements in the Arg1 promote”